Newsletter: Volume 7, Issue 2 August 2003

West Nile Virus

There’s a lot of talk this summer about West Nile Virus in dogs. Fortunately dogs seem to be pretty resistant to the virus. There was 1 confirmed dog case in Illinois last summer in which the dog died of neurologic signs. Heartworm disease is still the number one mosquito borne disease of dogs in our area. I’ve also been asked about mosquito control. Bayer has come out with a new product called K9 Advantix™ (you may have seen the commercials on TV). It kills and controls fleas, ticks and mosquitoes. It is a spot-on product applied to the skin on a monthly basis. This product is for dogs only NOT CATS. I’ve also recommended Avon’s Skin-So-Soft™ in a 1:20 dilution sprayed on the dog or cat as needed. Another product we have and I’ve used is Pet-Guard™ insecticide gel which can be used on dogs, cats and horses. It repels flies, mosquitoes and gnats. It is applied on the coat. Kiltix™ is a Bayer spot-on product which was introduced last year for tick control but also repels mosquitoes. Since there are excellent veterinary products for mosquito control I don’t recommend the use of human mosquito control products on dogs and certainly not on cats. Cats are very sensitive to insecticides and I would not use them on cats unless the label specifically states that it can be used on cats.

Common sense is also useful in mosquito control. Avoid leaving pets outside during times of high mosquito activity which usually coincides with the cooler times of the day — in the evening and early morning hours. I would not leave animals outside overnight without some sort of mosquito repellant on them.

I’m often asked if dogs can get West Nile Virus from ingesting carcasses of bird or other animals that may have died from West Nile. It appears that the tissues of dead animals are not a source of the virus — the mosquito is a necessary vector from transmission.

Certainly humans need to follow the recommendations of health officials regarding the prevention of human exposure. Have a safe and fun summer with your pets!


7-2a (9K)Colchicine has been proposed as a treatment for amyloidosis in animals. It has been used in man to prevent amyloidosis in Familial Mediterranean Fever. It apparently blocks the synthesis and secretion of serum amyloid A (an acute –phase reactant protein) by the liver thereby preventing the formation of amyloid-enhancing factor and preventing amyloid deposition. To be effective it must be given early in the course of the disease and it will be ineffective once kidney failure has occurred.

Colchicine should be used with caution in geriatric or debilitated animals. It should be used in during pregnancy only when its potential benefits outweigh its risks. Colchicine can cause nausea, vomiting and diarrhea in dogs. It may also cause abdominal pain and loss of appetite. Prolonged administration has caused bone marrow depression in people. Concurrent use with non-steroidal anti-inflammatory agents is not recommended.

I use 0.6mg. (1 tablet) twice a day in Shar-Pei with FSF, littermates with FSF or in lines with amyloidosis. If problems develop on colchicine therapy I stop the drug for a few days and then reinstitute therapy using a once a day dose or use half the dose twice a day. Once dogs become acclimated to the dog I try going with the full dose. Some Shar-Pei do not tolerate colchicine and can’t be on the drug. Also colchicine is used as a potential preventive for amyloidosis. It may or may not have an effect on the frequency or severity of the fever episodes.


Now that we are in the summer months I wanted to review one of the more common syndromes that we see in the news, read in the paper and witness here at the clinic — HEATSTROKE.

Before we talk specifically about this syndrome we need to understand a little about the normal control mechanisms that regulate body temperature. Normally the body maintains temperature within a narrow range called the set point. The thermoregulatory center in the brain controls body temperature by monitoring blood temperature via numerous heat sensors throughout the body. The initial response to increasing body temperature is activation of the panting center located in the brainstem.

Body heat is dissipated by four major mechanisms: 1) evaporation, 2) radiation, 3) conduction, and 4) convection. The primary operative mechanisms in the dog are radiation, convection and evaporation by panting rather than sweating as occurs in humans. At ambient temperatures below 90°F conduction, convection and radiation are effective in controlling body temperature. As the environmental temperature increases above this point evaporation becomes more important in maintaining body temperature. Evaporation occurs primarily through panting. A large portion of total body heat loss in dogs is due to radiation and convection from the body surface. The continuous movement of cooler air against the skin facilitates convection.

Two types of heatstroke are recognized: exertional heatstroke and nonexertional heatstroke. Exertional heatstroke is more common in late spring and early summer before dogs become acclimatized to high environmental temperature. Nonexertional heatstroke occurs when dogs are confined in an overheated enclosure or tied outdoors with no access to shade and/or water. This is understandable since heat loss mechanisms require ventilation (air movement), evaporation with subsequent water loss and behavioral mechanisms which cause the dog to seek a cooler environment. The most common cause of heatstroke in dogs is confinement in a vehicle! The second most common cause of heatstroke is seen in dogs tethered outdoors with no access to shade or water. In addition, should the dog become fouled up in the tether or entrapped in some other way, they panic and can become hyperthermic quickly and develop heatstroke.

Predisposing factors to heatstroke can be placed into two categories: decreased ability to dissipate heat and increased heat production. Conditions leading to decreased ability to dissipate heat include, lack of acclimatization, water deprivation, high ambient humidity and confinement with poor ventilation. Heatstroke rarely occurs in dogs that roam free. Heat dissipation can also be impaired by anatomic defects such as brachycephalic anatomy (stenotic nostrils, elongated soft palate, small diameter trachea), upper airway disease, neurologic disease, obesity, age and haircoat.

Heatstroke leads to severe damage involving the cardiovascular and respiratory systems, the central nervous system, the gastrointestinal tract, the hematologic and coagulation systems, and the musculoskeletal system. Changes to these important body systems manifest as heart rhythm irregularities, respiratory distress syndrome, pulmonary edema, brain damage, liver damage, acute kidney failure, coagulation problems such as DIC (disseminated intravascular coagulation, and muscle damage.

The most common clinical signs associated with heatstroke are elevated temperature usually 106°F or greater and excessive panting often accompanied by drooling. Neurologic signs also are common presenting as depression, difficulty in walking (ataxia), unconsciousness, inability to rise, etc. These signs are important in that other causes of fever such as bacterial and viral infections do not show excessive panting, drooling and neurologic signs usually. The key to the diagnosis is the history. The primary role of the owner is to recognize the signs of heatstroke and begin cooling measures as soon as possible, even before calling your veterinarian. The primary first step in treating heatstroke is to rapidly lower the body temperature to prevent damage to organs, but not rapidly enough to cause hypothermia. Every pet owner should have a thermometer which is for pet use and know how to use it — normal body temperature is 101-102°F. The dog should be sprayed down by the owner before transport to the hospital. Evaporation can be facilitated by placing the dog in front of a fan, driving with the windows open or placing the dog by the air conditioning vent. Cooling measures should be stopped when the body temperature reaches 103°F.

THIS IS A MEDICAL EMERGENCY! Get to the veterinary hospital as soon as possible safely. Medical treatment consisting of continued cooling, intravenous fluid therapy, and various drug therapies will be initiated immediately. Blood work will be collected including a complete blood count, blood chemistry screen, urinalysis and evaluation of blood clotting factors. Prognosis is guarded with dogs that die usually doing so within the first 24 hours. Complications of heatstroke such as kidney failure, heart problems, DIC, etc. can adversely affect the outcome.

Prevention is the most important owner responsibility. Owners need to consider the risk of exercising and/or confining dogs in hot environments. Be especially sensitive to taking dogs to the store and locking them in the car. Even cracking the windows is not safe enough and we all know how we can become distracted and forget about time! Heat stress can be prevented by providing adequate ventilation, a place where a dog can get out of the sunlight, free access to water, and a period of acclimation to hot weather.

Methylsulfonylmethane — MSM

7-2b (3K)MSM is a naturally occurring, organic sulfur-containing compound related to DMSO (dimethyl sulfoxide). MSM is found in small amounts throughout nature. Animal studies have shown that sulfur from oral supplements of MSM is incorporated into body proteins. MSM may be useful in the treatment of osteoarthritis in animals. Dose appears to be around 250-500 mg. per day. More research is needed before reliable recommendations for MSM supplementation can be made. Side-effects can include diarrhea, skin rash, headache and fatigue. It’s use in arthritis appears to be based on animal studies which indicate that joints affected by arthritis have a lower sulfur content. In humans a preliminary report concerning people with osteoarthritis, MSM reduced pain after 6 weeks.

The use of MSM for the treatment or prevention of Familial Shar-Pei Fever cannot be recommended at this time in my estimation. Certainly its use to replace colchicine as a preventative for amyloidosis is without merit.

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