An excellent resource that details all aspects of health issues for dogs, and one that every conscientious dog owner should have is: Carlson, Delbert G., DVM, and James M. Giffin, MD. Dog Owners's Home Veterinary Handbook (Revised and Expanded). Howell Book House, Macmillan Publishing Company, 866 Third Avenue, New York, NY 10022 USA (1992, 2nd ed). ISBN: 0-87605-537-4 (hardcover).
This comprehensive book is a complete guide to health care of dogs. It lets you know when you can treat the dog, or when you need to take it to the vet post-haste. It lists symptoms so that you may inform your vet of relevant information about its condition. The arrangement of the material facilitates rapid reference. Illustration of key procedures (pilling, taking pulse/temperature, etc). Lists poisonous substances, including houseplants. A must have home veterinarian handbook.
Other books/articles that you may find of use include:
Some help is available on VETMED, a moderated mailing list in which people ask about adn discuss veterinary problems -- not everyone subscribed is a veterinarian, of course, but quite often people here can point you to where you should look. Email to firstname.lastname@example.org with SUBSCRIBE VETMED yourfirstname yourlastname in the body of the message. Be sure to substitute your own first and lastnames in the subscribe command.
Addison's Disease (hypoadrenocorticsm or adrenocortical insufficiency) is an uncommon but potentially fatal disorder in which the adrenal glands do not secrete enought gluco- and mineralo-corticoids. Without these hormones, death will occur. The symptoms are vague and non-specific, so it's easy for the disease to become life-threatening before it is diagnosed.
Symptoms include depression, weakness, vomiting, diarrhea, dehydration, weight loss and shivering. A veterinarian may find decreased mental ability, a slow heart rate, poor pulse quality, and low body temperature. Blood tests may reveal increased kidney indices and electrolyte imbalances of low sodium and chlorine and high potassium. A simple test called ACTH stimulation confirms the disease.
Treatment traditionally involves replacing mineralocorticoids with fludrocortisone acetate (Florenef Acetate); glucocorticoids may also be replaced depending on the dog's condition. Dogs tend to be resistant to the desired effects of Florenef, thus high doses are required and side effects include increased thirst, urination, and urinary incontinence in some cases. An experimental drug that may soon be approved for use in animals is desoxycorticosterone pivalete (DOCP, available through Ciba Animal Health) injected subcutaneously. Preliminary studies are encouraging, and details may be found in JAAHA March/April 1995.
(summarized from Carlson & Giffin)
Normally, anal sacs are emptied when the dog defecates. Some dogs with overactive anal glands may require occasional help. Your vet can demonstrate the procedure.
A common indication of trouble with anal sacs is "scooting" (dragging the rear on the ground).
Impaction: occurs when the anal sacs fail to empty properly. This is more common in smaller breeds. Squeezing the sacs yourself as needed will control the problem.
Infection: complicates impaction. There is blood or pus in the secretions, and the dog may scoot (drag its rear on the ground). It may be painful. Check with your vet for an antibiotic you can apply after you empty the sacs.
Abscess: Signs of anal infection, with a swelling at the site of the gland. It goes from initially red to a deep purple. You will have to have it lanced and cleaned by the vet.
Dogs whose anal sacs become repeatedly infected and/or abscessed will need to have the glands removed. Surgery is uncomplicated, although the dog will have poor bowel control for the next few days after surgery. Try putting a pair of small boy's underpants, with the dog's tail through the third opening, on the dog to contain accidents.
How dangerous is anesthesia?
While anesthesia is not without risks, it is most certainly not guaranteed death for your dog. Your vet anesthetizes dozens of animals a week without losing them, and your pet should be no exception. There are a number of different anesthetics available, each with their own benefits and risks:
This is just about archaic and should not be in much use any more. Some vets still use it because it is inexpensive, but it is not as safe as newer anesthetics available today. Halothene
Probably the most commonly used. It is a good general purpose anesthesia which is simple to control. A drawback is that it takes animals up to an hour to completely wake up from it and they usually behave sedated for up to another 12 hours. The only real reason to use it now is that it is less expensive than isoflurane. Isoflurane
Extremely safe, produces complete anesthesia for any type of surgery and it is not metabolized by the kidneys in the same manner as halothene or methoxyflurane.
What can I do to improve the odds?
The greatest danger from anesthetics is improper processing of the drug by the dogs metabolism. All these anesthetics are eliminated from the blood stream through the liver and kidneys. Older dogs in particular can have defects in these organs that can cause complications under anesthesia. If you are concerned about this your vet can do a preliminary blood panel to detect potential problems. If your pet has a heart murmur or a respiratory problem make sure your vet is aware of it. These are not necessarily problems during anesthesia, but will allow your vet to make an informed decision should a problem arise. You should also ask your vet if sie knows of any problems peculiar to your breed. Sighthounds in particular are more sensitive to anesthetic and require lower levels to achieve the same effect. Make sure that you keep a complete medical history of your dog and that you take a copy of it with you whenever you change vets.
Why is anesthesia used for OFA X-rays?
Most Xrays can be taken without any sort of sedation, but OFA Hip X-Rays require certain amount of stretching and twisting of the legs to get the hips into a proper position. Most dogs will struggle from the handling (or in some cases, pain if they are dysplastic), and the resulting X-rays can end up blurred. While for many cases this would be OK, OFA requires very sharp images. It is possible (as has been mentioned here often) to get acceptable X-rays without sedation or anesthetic, but it requires a lot of work and experience along with a cooperative dog and this may miss some borderline cases.
Autoimmune Hemolytic Anemia (AIHA)
This disease is only partially understood at this time. See also http://www.vetinfo.com/dimmune.html#IMHA.
Blood transfusions are the topic of much controversy. One school of thought is that the animal is likely to hemolyse the transfusion, so blood should be tranfused only in lifethreatening situations. The other school argues that transfusions have never been proven to be dangerous in this disease (and goes on to assume that they are therefore safe).
There are two types of AHA: primary, where the system destroys its own red blood cells for no apparent reason, and secondary, where the red cell membrane is changed (perhaps by a virus or parasite) and is then destroyed as abnormal. Prognosis for secondary AHA is much better and depends on how well the underlying cause can be treated. The prognosis for primary AHA is much worse, with only 50% of the animals living beyond 12 months.
Dogs that breath noisily may have a serious health problem. For example, some animals have an elongated palate, which prevents them from breathing properly. The animal can also have a hard time drinking and eating. This also can affect the heart since it has to work extra hard to breath.
If your dog has this problem check with your vet. There is an operation that can correct the problem of elongated palates. In any case, dogs should not be constantly panting and breathing noisily, so a vet check is in order. In general, breathing anomalies should be investigated: noisiness, wheezing, excessive panting, excessive coughing.
Blood in the stool can appear in several ways, each indicating a different problem. Black stools mean bleeding high up in the digestive tract, most likely a bleeding stomach ulcer. Reddish stools indicate blood further down the pipe, after the digestive juices have been neutralized somewhat. This can be anything from ulcers in the small intestine to ulcerative colitis. Red blotches/streaks on the surface of the stools (with normal color otherwise) indicate bleeding in the last segment of the large intestine or rectum, after the stool has begun to solidify (the function of the large intestine is to neutralize digestive juices and absorb liquid). This can be ulcerative colitis (or some other inflammatory bowel disease) or bleeding hemorrhoids. Each of these problems can be very serious, and in some cases life-threatening (with the exception of hemorrhoids).
Coloring (natural or artificial) in food can also directly color the stool so you can't be sure of anything without a chemical analysis. A sudden diet change/addition can also affect stool color. Get a sample to the vet.
Brucellosis is one of the few venereal diseases among dogs. It is associated with testicular atrophy. It causes sterilization (sometime obvious, sometimes not) in the male, embryonic reabsorption, abortion, weak pups that die soon after birth and eventual sterility in females. Males are contagious for months through their semen, females are contagious for several weeks after the failed pregnancy.
Brucellosis may be passed to humans. It can cause suppressed immune systems and sterility in humans. However, brucellosis in this form cannot be passed back to animals or other humans, as this disease is not adapted to humans.
Diagnosis can be quickly made, although animals tested less than three weeks after exposure will show negative. False positives are possible; followup diagnosis with more reliable methods should follow any initial positives.
Treatment for brucellosis is not generally very successful and often very expensive. Extensive antibiotic therapy, evaluation and additional testing will add up quickly, with no guarantee of success. No vaccine is available.
Any animal with brucellosis should not be bred, and should be eliminated from the kennel or other breeding stock before infecting the entire colony. Animals entering the breeding area, male and female, should be tested for brucellosis PRIOR TO breeding.
Canine Parvovirus (CPV)
This is a recent disease, first noted in the late seventies. It is highly contagious and puppies have the highest mortality. There is a vaccine available, and you should make sure your dog is up on its shots. In some areas where parvo is prevalent, you may need booster shots every six months instead of every year.
Parvovirus comes in several forms:
(summarized from Carlson & Giffin)
In the US, there is a current upswing in Parvo infections. Make sure your dog is up-to-date on its vaccinations. Don't let a too-young puppy roam where possibly infected dogs have been (for example, in the park). Contact with feces or un-vaccinated dogs is the primary source of transmission. Some breeds seem to be especially sensitive to parvo, such as Rottweilers.
Chondrodysplaysia was discovered around 1930-1940s. This disease is neither "dwarfism" as it is commonly referred to nor is it dysplaysia (in the true sense of the word). This debilitating disease is actually a birth defect causing the dog's upper foreleg to become overly massive, short, and twisted and appears in Malamute and related breeds. Malamute breeders were appalled by this condition when it appeared and immediately set out to eradicate it.
Steps were taken to locate these recessive genes. By breeding an unknown dog to a known CHD, the pups were then rebred to CHD dogs and percentages were calculated. Most Malamutes today have been CHD rated. The percentage is the actual likelihood of CHD showing up in a breeding. Malamute breeders tend to agree that 6.25% (one great-great-great grandparent is a carrier) is the upper limit of acceptablity in a CHD rating.
Puppies are CHD rated now by taking the CHD factors of both parents and averaging them together. Example:
(1.75 + 2.01)/2 =
Needless to say, an non-CHD certified Mal or a Mal that is certified above a 6.25% should not be bred, in order to contain the disease. Non-CHD certified dogs can be CHD certified, but it is a very expensive procedure.
CHD may be diagnosed with various tests that include blood tests and x-rays. The Complete Alaskan Malamute by Riddle and Seely covers this disease fairly well.
Coccidiosis is caused by protazoal parasites of either Eimeria spp. or Isospora spp. Crowding, poor sanitation, or stress may facilitate its spread.
Symptoms depend on the species of protozoa, the infective dose, and the amount of damage caused. They can range from mild diarrhea to severe, bloody diarrhea with subsequent dehydration and anemia. Following infection, the affected animal may become a carrier. Coccidiosis is a cause of diarrhea in puppies. It may result in death in puppies.
Treatment consists of supportive therapy once disease develops. Drug therapy is ineffective - all of the available agents are coccidiostatic agents; they can prevent infection, but will not treat an established infection. Good sanitation is essential in preventing coccidiosis. Most disinfectants are ineffective against coccidian oocytes, but boiling water and 2% formaldehyde are effective if they reach the oocyte. Scrupulous cleanliness is the best preventive, although it is no guarantee against Coccidiosis.
Because coccidia is an environmental contaminant that produces an opportunistic infection, stress of any kind, such as vaccination, may be all that it needs to manifest. Adult dogs are carriers, and the coccidia oocysts are pretty resilient to most common disinfectants. Coccidiosis may be a major problem in an unclean environment, but may crop up a well run operation as well. An adult carrier will serve as a potential source of infection to puppies. The fact that a kennel has problems with coccidia is not itself a scathing indictment of the kennel - it's just a fact of life that has to be dealt with.
While some dogs certainly become deaf through illness, trauma, or old age, most dogs are deaf through heredity. Some of the breeds most affected by this problem include Dalmatians and English Setters. Many of the pigmentation genes are connected with deafness. For example, blue eyes and deafness are statistically associated to a high degree of certainty. Lack of corneal pigment is also connected. Since a puppy with only one unilaterally deaf parent is twice as likely to be deaf as a puppy with both parents hearing in both ears, any dog that flunks the BAER test should not be bred.
The definitive test for assessing a dog's deafness is the BAER test, which can tell whether a dog is unilaterally (one ear) or bilaterally (both ears) deaf. In breeds where deafness is a problem, you should insist on a puppy that has been BAER-tested.
There is a mailing list for owners of deaf dogs that can help you answer many of your questions (mail email@example.com for information). In addition, you should look at their informative web site, http://www.cybervision.com/~cairo/deaf.html.
Degenerative Joint Disease
DJD = Degenerative Joint Disease (osteoarthrosis): DJD is a degeneration of cartilage that can either occur as a primary condition in older animals as a result of normal wear & tear, or as a secondary condition to any other condition that affects a joint and surrounding structures. It is not an inflammatory condition, as opposed to infectious forms of arthritis or immunologic forms of arthritis (rheumatoid arthritis or systemic lupus erythramatosus).
DJD can be ruled out with radiographic analysis such as OFA or Wind Morgan provide.
(summarized From Carlson & Giffin)
Distemper is the leading cause of infectious disease death in dogs, most commonly in unvaccinated puppies 3-8 months of age. Among infected dogs: half show little in the way of illness; many show mild symptoms; and in a few the illness is severe or fatal. Malnourished and ill-kept dogs tend to show more acute forms of the disease. Secondary infections and complications with distemper are common. Prognosis depends on how quickly the dog is diagnosed and treated, and which form of the disease the dog has.
There are two stages. Symptoms in the first stage include fever, loss of appetite, listlessness, and a watery discharge from the eyes and nose. It may appear like a cold -- but dogs do not get colds the way people do; a "cold" is therefore much more serious in a dog than in a person. Within a few days the discharge will thicken: a primary indication of distemper. Dry cough, pus blisters on the stomach, diarrhea (and associated dehydration) may follow. At this point, the dog may recover, or proceed on to the second stage which involves the brain. Dogs with brain involvement do not usually survive.
"Elbow Dysplasia" is a general term that includes any of several conditions:
Evidence that both OCD of the elbows and FCP are heritable in at least one breed was discussed in "The Inheritance of Osteochondritis Dissecans and Fragmented Coronoid Process of the Elbow Joint in Labrador Retrievers" by GA Padgett, UV Mostosky, CW Probst, MW Thomas, and CF Krecke, published in the Journal of the American Animal Hospital Association, Vol. 31, pp 327-330. Test breedings showed and increase in both OCD and FCP when selected for, demonstrating a genetic potential. However, as normal siblings were also produced, this condition is not a simple recessive. Most probably it is a polygenetic trait, similar to Hip Dysplasia, with the attendant difficulty of removing from the gene pool. As of this writing, early screening for these conditions in the breeding stock is strongly advised to eliminate dogs with this condition. In addition, littermates and close relatives of affected dogs should be reconsidered as good breeding stock, as they are likely to carry some of the genes for these conditions.
The paper focused on Labrador Retrievers; however it is quite likely that as with Hip Dysplasia, Elbow Dysplasia is heritable in a number of other breeds as well.
Osteochondritis Dessicans Osteochondrosis dissecans affects dogs of the large, rapidly growing breeds between the ages of four and twelve months. It usually is found in the shoulder or elbow joints, but rarely it can affect the hocks or stifles. It is due to a defect in the cartilage overlying the head of one of the long bones. A puppy who jumps down stairs might sustain such an injury. The tendency for cartilage to be easily damaged may be hereditary. Repeated stress to the joint perpetrates the condition. The signs are gradual lameness in a young dog of one of the larger breeds, typically between six to seven months of age.
The lesions primarily affect cartilage and secondarily bone, and can occur in the elbow, shoulder, hock, and/or stifle, though the elbow is by far the most common. When the condition is associated with inflammatory joint changes it is known as OCD.
Pain is present on flexing the joint. X-rays may show fragmentation of the joint cartilage, or a loose piece of cartilage in the joint.
OCD in the elbow has been proven in the Labrador to be hereditary, but no such proof has been shown for other forms of OCD or heritability in other breeds. However, it would be prudent to assume that outside of traumatic origin, a polygenetic mode of inheritance is at work.
Surgery is indicated to remove the pieces of cartilage, smooth both the top of the joint and the cartilage to stimulate new growth without flaps or chips. Recovery and prognosis are generally very good; there are many cases of dogs who had this surgery and went on to compete in obedience and agility once completely recovered. However, no matter how sucessful the surgery, the dog should not be bred if a hereditary cause is suspected.
Fragmented Coronoid Process Ununited Anconeal Process
Ununited anconeal process has been known for quite a while in in the German Shepherd Dog, but can also occur in other breeds (Dobermans and, increasingly, Golden Retrievers) It is really only one part of a constellation of problems collectively referred to as elbow dysplasia.
This is a serious condition because it usually results in arthritis and efforts need to be made to be sure that the dog has enough exercise to keep fit, but not so much or of the wrong kind that would make the arthritis more severe. The condition should be handled surgically by an experienced orthopedic specialist.
It is thought to be genetic, and OFA now certifies dogs based on X-rays in the belief that its incidence will be reduced this way.
Diagnosis and Registry Any of these conditions must be diagnosed via radiographic analysis. OFA will certify elbows on dogs 24 months of age or older. Abnormal elbows are reported as:
Following are short synopses of the most common forms of eye problems.
CEA (Collie Eye Anomaly) is the most common form of eye problem found in the collie, both rough and smooth variety. It is also found in the border collie, shetland sheepdog, and bearded collie. It is believed to by controlled by a genetic cluster, or large group of genes, and thus, it is hard to control by breeding, and ranges in severity.
PRA PRA (Progressive Retinal Atrophy) is common in MANY breeds of dogs (including mixed breeds), and is not isolated to the collie like the CEA tends to be. PRA affects the entire retina and is the canine equivalent of retinitis pigmentosa. This disease manifests itself differently in different breeds. The most common form of PRA in the collie is detectable at early age (6wks and over). The form of PRA in Irish Setters is also early-onset. In Labrador Retrievers, on the other hand, the age of onset is much later, typically four to six years of age, making it much harder to find and isolate carriers in this breed.
PRA has been detected as early as six weeks in puppies, and these puppies are usually blind by six to eight months. An electroretinography can be used to detect the early signs of PRA. Animals to be tested in this manner are anesthetized while lenses are placed on the eyes to record the retina's reaction to light. (Like wearing contacts.) In other cases, ophthalmological examination by ACVO-certified vets can pick up cases of PRA and confirm them with electroretinography if desired.
All dogs affected with PRA eventually go blind. Carriers show no clinical symptoms. Symptoms are subtle, starting with night blindness, some eye dilation, to progressive blindness. It's quite common to not notice anything is wrong until the dog is nearly completely blind. Proactive testing is always recommended, especially for breeding stock.
Current research is beginning to isolate the genetic markers for this disease. At present, there is a genetic test to identify carrier and affected dogs in the Irish Setter breed. Work is underway for one for the Labrador Retriever. This disease is thought to be a simple autosomal recessive gene. Thus two recessive genes are needed for a dog to be affected. A single recessive gene masked by the healthy dominant means the dog is a carrier. Therefore, an affected dog's parents are carriers or also affected.
NOTE: In October 1945 the Kennel Club of England added PRA to the list of disqualifications from winning any award in the show ring.
Glaucoma This is a condition where the pressure of the fluid in the eye increases until the sight is gone in that eye. If it strikes one eye, the other eye is likely also to be affected. Glaucoma is one of the leading causes of blindness in dogs. Any underlying problem that increases the fluid pressure inside the eye is the culprit; most of the time this is due to inadequate drainage of fluid from the eye (as opposed to overproduction of fluid). A few forms of glaucoma are thought to be hereditary.
Signs of glaucoma include reddened conjunctival tissue (red eye), weeping, light sensitivity, or even enlargement of the eye. As pressure increases, the pupil can become dilated and the cornea cloudy. Early diagnosis is critical to save the vision of the dog, and involves treating the underlying causes of the increased pressure if at all possible.
There are several options in treatment, which depend on the extent to which the eye has been damaged, and the amount of vision that has been lost. In addition, some dogs will respond better than others to medications:
Cataracts may be stable or progressive. In the former case, owners may never be aware that their dog has cataracts until or unless the dog is examined. In the latter case, the dog often adapts very well to the gradual loss in vision until a certain point is reached. General diagnosis can be done by ophthalmoscopic examination; if a more detailed examination is needed, a slit lamp examination must be performed.
Surgery is the only option for cataracts that seriously impair vision. Most surgery involves removal of the lens; however, implants can also be performed. Recovery and prognosis for these dogs are generally good.
There are several types of Retinal Dysplasia:
If we bred NN x Nrd we would expect half of the puppies to be affected the others normal. If we bred Nrd x Nrd we would expect the following:
In mild cases of retinal dysplasia, sight is probably not affected much, if at all. In severe cases, skeletal abnormalities are present.
To avoid confusion, do not move your furniture around (except for any piece that the dog does keep bumping into. Be sure the dog knows when you are near so it is not startled. When you go out on walks, establish habitual trails. Your dog will adjust quickly.
For more information on Canine Eye disease contact:
Vanderlip, Sharon Lynn, DVM. The Collie: A Veterinary Reference for the Professional Breeder.
Rubin, Lionel F. Inherited Eye Diseases in Purebred Dogs, Williams & Wilkins, Baltimore, 1989.
CERF Publication "Ocular Disorders Proven or Suspected to be Hereditary in Dogs". The publication can be ordered directly from CERF by calling their office at (317) 494-8179.
Gastric Dilation and Bloat
A condition more commonly seen in larger breeds. Gas in the stomach causes it to swell. In some cases, the stomach rotates on its axis, closing off both ends of it. Digestive processes continue unabated and the stomach swells up. The cause of bloat is unknown.
Some forms of bloat are fatal untreated; survival depends on understanding what is happening and getting the dog to the vet, the earlier the better.
History is important: in nearly all cases, there is a history of overeating, eating fermented foods, drinking excessively after eating, or taking vigorous exercise after a meal (within two or three hours).
If your dog is able to belch or vomit, it is more likely a gastric upset. If it cannot, rush it to the vet or emergency care NOW for emergency surgery.
If your dog is at risk for gastric bloat, you should discuss it with your vet before a possible episode. Your vet may recommend (and demonstrate) some things you can try to do as life-saving measures while getting it to the vet.
Measures thought to reduce the risk of gastric torsion ("bloat"):
Giardiasis is a malabsorptive syndrome. The parasites adhere to the lining of the small intestine where they interfere with absorption of nutrients. Light cases of Giardia often go undetected and many dogs "self cure" by expelling and developing an immunity to the parasite. In heavier infections, Giardia can interfere with absorption of certain types of nutrients, especially fats and certain vitamins. Fats are not absorbed and result in excess mucus in the stools which are very pungent and diarrhetic.
The parasites interfere with normal metabolism by forming a physical barrier between the lumen of the intestine and the absorptive cells. Excess mucus results from malabsorption of fats while excess water results in the diarrhea. The intestinal lining is not usually injured so stools should not contain blood.
The parasites feed on partially digested food in the lumen of the intestine. They do not compete directly with the host for food. Their metabolism is primarily anaerobic, meaning that they do not utilize oxygen in their respiration. They lack cellular organelles concerned with aerobic respiration such as mitochondria.
The active stage within the host is the trophozoite (feeding body); this is the only pathological form. The transfer stage of the parasite is the termed the cyst. Giardia forms cysts by extruding cellular food particles and other vacuoles and secreting a resistant cyst membrane around the cell. This highly resistant cyst is then passed from the host in the feces. Trophozoites may be passed but quickly die. Cysts that are passed into water can survive for an extended time, up to 1-2 months under proper conditions. Survival times on land are somewhat less. A new host becomes infected by drinking fecally contaminated water or eating the feces of an infected animal. While food-borne transmission is rare, it has been documented for humans. Dogs may become infected by drinking out of streams, lakes or ponds containing Giardia cysts. Other sources of infection are wild animals that visit the kennel area and deposit infected feces in an area accessible to the dog. Scats of other dogs or wild animals are potential sources of infection for domestic dogs. Giardia is potentially transmissible to humans so caution is warranted.
Giardia can be difficult to detect even for professionals. It is too small to be seen by the unaided eye. A high quality microscope is needed for proper diagnosis; phase contrast microscopy is helpful. A definitive negative diagnosis should include stools collected on multiple days since cyst production tends to be cyclic with millions produced one day and few the following day. The cyst is the diagnostic stage of Giardia. Cysts tend to be approximately 9-15 micrometers in length and 4-5 um in width. Cysts are identified by size, the presence of four nuclei, axostyles and claw-hammer shaped median bodies.
The current drug of choice is metronidazole, known by the trade name FLAGYL. Although highly effective it is a known carcinogen and mutagen in mice. Quinacrine (ATABRINE) can also be used but is not as effective. Treatment is usually one tablet per day for 7-10 days, depending on the weight of the dog. Recovery is usually uneventful but a dog may become reinfected after treatment. Thus, it is important to try to isolate and eliminate the source of infection.
New in treatment is Panacur (FENBENDAZOLE). Panacur has been more effective than metronidazole in recent years.
Symptoms may not appear until a full year has passed since infection. Because of this, the disease is often mistaken for another problem. The most persistant sign is a soft, deep cough. After exercise, the cough may be so severe that that the dog faints. Weight loss, discharge of bloody sputum, listlessness, and weakness are also common (from Carlson & Giffin).
The Heartworm Lifecycle
Start with an infected dog. This dog has adult heartworms living in its pulmonary arteries (they crawl into the heart after the dog dies). Female worms mate with male worms and produce microfilaria (first stage larva, L1, or a "baby" heartworm). The microfilaria enter the circulation of the dog. When this infected dog with circulating microfilaria is bitten by a mosquito, the mosquito will ingest 1 or 2 microfilariae. If the mosquito ingests more larvae than this, it will die!
In the mosquito, the microfilariae (L1) will molt twice, to the L2 and then the L3 stage. At the L3 stage, the larvae migrate to the mosquito's mouthparts. Then when the mosquito bites a dog, the larvae are deposited ON the dog's skin and then crawl into the bite wound left by the feeding mosquito. If a mosquito with the L1 or L2 larval forms bites a dog, they will NOT be transmitting heartworms to the dog. Likewise, if the L1 forms are not removed from the dog's circulation by a biting mosquito, they will die off. The L1 stage does NOT "mature" into adult worms in the dog. So, the L3 larvae that crawl into a dog bitten by a mosquito will develop in the dog's subcutaneous tissues to L4 and finally L5 life stages. These then enter the venous system and enter the heart. They travel to the pulmonary arteries and become full-fledged adult worms, ready to reproduce.
General principles of heartworm testing:
When a dog is tested for heartworms, a sample of blood is drawn. The blood cells are lysed and the remaining sample is examined microscopically for the presence of microfilariae. (This is the Knott's test or Filter test, depending on how it's done). So, if no microfilariae are seen, the dog is diagnosed as being heartworm negative and you can restart medication. Because of the development that the larvae must go through prior to becoming adult worms and reproducing, it takes, on average, 6 MONTHS from the time a healthy dog is bitten and infected until the dog has circulating microfilariae. This means that a heartworm test done less than 6 months since a dog was bitten and infected will be *negative.* Dogs that have been taking Heartgard present another problem in the detection of heartworms. Heartgard will cause adult female worms already present in the dog to become sterile, so the females will not produce any microfilaria. Heartgard will not kill any adult worms. The adult worms cause heart problems with dogs who have heartworms, NOT the microfilariae. It is the adult worms that we are really attempting to protect the dog from when we use preventative medication.
So if a dog is on Heartgard and is tested for heartworms using the Knott's test, chances are the dog will test negative even if there are adult worms present.
There is a different, more expensive test for dogs who may have sterile worms. It uses a blood sample to test for antigens produced by the adult heartworms. If the dog has heartworm antigen, it has a greater than 99% chance of having heartworms. This test should be used on any dogs that are on Heartgard since they will not have microfilariae in their bloodstream. Likewise, if there are only low numbers of circulating microfilariae, the Antigen test will give a positive result where the direct Knotts (Filter) test may be negative. Just like the standard Knotts test, the Antigen test will be negative if the dog was infected less than 6 months ago.
It is therefore very important for those dogs on the monthly medication to be tested with the Antigen test rather than the Knotts!
Can another dog can get heartworm by coming in contact with an infected dog's blood? (transfusion, bite)
The monthly medications are Heartgard and Interceptor. Heartgard is Ivermectin and Interceptor is Milbemycin Oxime. These medications work by killing any larvae that have entered the dog up to 45 days ago. They kill L3s, 4s, and 5s.
These drugs are given monthly (30 days) for the convenience of giving on the same day each month and also to give you a safety margin. If you forget to give your dog his/her heartworm medication, you have about 15 days to remember to give it and the dog will still be protected. With the daily medication, forgetting for more than a day may result in your dog becoming infected.
Most common ways that a dog will contract heartworms while on medication include not being given medication on a regular basis (e.g. completely missed dosages); traveling from a winter environment to a summer environment like Florida without giving the dog heartworm medication; not WEIGHING the dog while on the medication: the dog outgrows its dosage; and the dog vomiting or having severe diarrhea after being given its medication.
What should you do if you forget your dog's medication?
*IF* the dog is on daily medication, give the dog a monthly tablet within 45 days of the missed dose. Depending on what you feel comfortable with, you can then restart the dog on the daily medication, or continue giving the medication once a month.
*IF* your dog is on monthly medication, give the medication anytime you remember, even if more than 45 days has passed. Giving heartgard to a dog with heartworms will not hurt the dog, and until 6 months has passed the dog will appear to be negative anyway. However, you should NEVER give daily medication to dogs who may have circulating microfilariae. The daily medication can cause an anaphylactic reaction if given to a dog with microfilariae present. Giving monthly medication will prevent the dog from acquiring a heavy worm load by being bitten by multiple infected mosquitoes. Just be certain to have the dog tested 6 months after the missed dose to be sure that the dog did not acquire heartworms.
Treatment Of Heartworm Disease
Treatment for heartworms is difficult on the dog and prevention is easy. If your dog tests positive for heartworms and you decide to treat it, here is what will happen: Your vet will want to take a blood sample to begin with to check the dog's liver function. The treatment that kills the adult worms uses a drug called Caparsalate. This drug is given twice a day for 2 days while the dog is in the hospital. The dog must be kept quiet (caged) for 4 weeks after the adult worms have been killed. It takes 7 to 17 days from the time of treatment for the adult worms to die. Within this time, dead worms will fragment and travel to the dog's lungs. If dead worms are numerous, some of the blood vessels to the lungs will become blocked, and this is inevitable. However, if the dog is kept quiet and only allowed to move around enough to go outside, the blockage of pulmonary vessels may remain subclinical. If the dog is allowed to run around, the heart rate increases and many dead worm fragments will travel to the lungs at the same time. This is what you want to avoid.
About 4 weeks after Caparsalate has been given, the dog will be given a high dose of ivermectin to kill the remaining microfilaria that are circulating. Although this is a high dose of ivermectin, it is below the lowest dose known to cause mild, self-limiting toxic side effects in Collies. Obviously, after being treated, dogs should be kept on heartworm preventative! As of 1997, there is a new treatment method for dogs with heartworm. I have been informed that Immiticide (Melarsomide) is an intramuscular injectable heartworm treatement that obsoletes Caparsolate.
Summary Of Medication
Heartworm preventives include ?
A Guide for Dog Breeders and Owners
2nd Edition 1989
By E.A. Corley and G.G. Keller
A single copy is available for a donation and multiple copies are $3.00 each at Orthopedic Foundation for Animals, Inc, 2300 Nifong Blvd, Columbia, MO 65201, 573-442-0418. It is informative, and highly recommended.
Another good source of information on Hip Dysplasia may be found in the chapter "Hip Dysplasia" in Genetics of the Dog by Malcolm B. Willis (Howell Book House). Information from this chapter is also presented below.
In general Hip dysplasia ("bad development") appears in people and many species of animals. In some breeds of dogs, it is the most common cause of osteoarthritis or degenerative joint disease. Because both humans and dogs get hip dysplasia, dogs made a good subject to use in research. Most of these techniques below are also used on humans.
Research on hip dysplasia suggests that CHD is a more complex disease than was first thought. There are no simple answers or solutions to the problem. The complexity of CHD results in research findings that appear to be contradictory. However, many aspects of the disease have been repeatedly and independently documented and are generally accepted by the scientific community. Three important ones are:
The early changes are not easily detected. Severe cases may be diagnosed as early as 7 weeks of age; others may not show up in radiographs until over 2 years of age. This is why OFA only certifies dogs over two years of age.
Breeding Most inherited traits in animals are polygenic. These traits do not follow patterns based on dominant/recessive pairs because polygenic traits are affected by many genes. Only some puppies will have the same combination of genes for a trait as the parents. Some will have a more desirable combination while others will have a less desirable pattern. As the number of involved genes increase, the possible outcomes also increase. In addition, remember that it is also possible for different genes to have a different level of influence on the trait, complicating the outcomes considerably. Predictions of a specific outcome from a particular mating involving polygenic traits is currently impossible.
In Corley and Keller's opinion, a dog with excellent hips but with more than 25% of its brothers and sisters affected with hip dysplasia is a poorer breeding prospect than a dog with fair hips and less than 25% of its brothers and sisters exhibiting dysplasia.
(from Corley & Keller)
"...[T]he signs [of hip dysplasia] vary from decreased exercise tolerance to severe crippling. They include: a reluctance or inability to go up or down stairs, difficulty in rising from a sitting or prone position, bunny-hopping gait when running, stiffness early in the morning that improves as the dog warms up, change in disposition due to pain, lameness after exercise, wobbly gait, a clicking sound when walking, and many others. Many dogs will shift their center of gravity forward in an effort to relieve weight and pressure on the hips. These dogs generally present a front end that appears well-developed relative to the rear end.
"In dysplastic dogs, the hip joint is a weakened structure that is more subject to being injured by normal activity such as jumping off a couch, or rough housing with a playmate. Frequently, this results in an acute lameness that in the mind of the owner was caused by the injury, whereas the underlying dysplasia actually made the joint more susceptible to injury. Obviously, the normal hip can be injured, but the radiographic examination can usually distinguish between a hip problem due to dysplasia and one due to other causes.
"CHD can not be diagnosed by observing how the dog moves, acts, lies down, etc. The clinical signs may be caused by other problems; therefore, a complete orthopedic and radiographic examination is required before arriving at the conclusion that the signs are caused by CHD."
Environmental factors such as type of food and exercise in puppyhood have been shown to affect the displayed symptoms within the same litter. However, subsequent generations from both groups showed the same rates of dysplasia meaning that while the phenotype may be affected, the genotype is what determines whether a dog has the potential for being affected with HD.
In general, low protien diets and low activity levels through puppyhood reduced the symptoms of HD markedly. However, the degree of diet reduction and no activity may or may not be practical for the average dog-owner to attempt. (See Willis.)
It's best to keep your puppy from any kind of jumping for the first year or so in life. It's also best to keep from sustained exercise until at least a year old. Sustained exercise includes: jogging with owner, pulling weights, mushing, running with owner on bike, etc. Even for dogs not at risk from HD, it's wise not to exercise too strongly too early as such exercise may interfere with proper growth of joints, leading to similar problems such as arthritis on the joint or OCD.
Diagnosis of Hip Dysplasia Any diagnosis of Hip Dysplasia must be made via expert radiographic diagnosis. This involves taking xrays of the joint and typically sending the film to organizations that will evaluate, register, and certify the dog. Veterinarians will often "diagnose" the film themselves but if the question is critical its best to have them properly evaluated (unless, of course, your vet is experienced with radiographic evaluation -- not all are).
You cannot, repeat, cannot make a reliable diagnosis of Hip Dysplasia on the basis of external symptoms such as lameness or gait.
The Orthopedic Foundation for Animals is the most well known registry in the United States. It grades all joints, most commonly hips, as severe, moderate, fair, good, and excellent. It will certify all passing grades given to dogs over 2 years of age. Contact: 573-442-0418.
PennHIP is a new evaluation technique that flexes the limbs differently to produce the xray pictures. There are only a handful of vets around the country that have been certified to take xrays using the PennHip method.
Genetic Disease Control, UC Davis
There is a program here for radiographic evaluation of dogs. Wind Morgan is the most well known of these programs, offered to Labrador Retrievers. There are similar programs for Rottweilers and a few other breeds. Wind Morgan will certify at one year of age or older and requires xrays of hips, elbows, and hocks. They will hold clinics around the country to help hold costs down.
Genetic Disease Control is a larger effort to collect data on all kinds of genetic diseases, of which Hip Dysplasia is only one. They have registries and information on a wide array of diseases. All their registries are open, in an effort to make more information available to breeders in making informed choices about their breeding stock. For more information, write to
PO Box 222
Davis, CA 95617
Outside the United States
Each country typically has its own hip evaluation program. These are not consistent from country to country and may differ with the evaluations give by the above US organizations. In Australia, dogs are evaluated by the Australian Veterinary Association that has an Australian wide scoring scheme with averages for each breed.
Life for dogs with Hip Dysplasia First of all, be sure that your dog has been accurately diagnosed with HD. Many vets do not have the expertise in reading the x-rays, so you need to be sure that an experienced radiologist reads them. If you're not familiar with the competencies of the vets in your area, your best bet is to have the x-rays sent in to OFA for evaluation. You CANNOT definitively diagnose HD on the basis of external appearance or palpitation of the joint or anything like that. Many things can cause limping, some of which are correctible, so it pays to be certain you have the correct diagnosis.
Diagnosis of Hip Dysplasia is not an automatic death sentence for your dog! Because it is a polygenetic trait, the variability of expression is actually quite wide. Some dogs may experience little or no discomfort and you may never know they have HD unless you test for it. Other dogs may experience more pain, but it may be easily controlled with proper exercise and judicious use of aspirin under the direction of a vet. Only a small percentage of cases are so crippled by HD that they must be put down.
You should immediately neuter any dog that has HD. The only known means of eliminating this disease lie in well-managed breeding programs, so do your part by eliminating the possibility of your dog contributing to the overall problem.
Discuss with your vet appropriate strategies for dealing with HD. In most cases, the general advice is to keep the dog from doing any kind of jumping or causing other sudden stress to the joints. However, as solid muscle buildup around the joint helps to ease the pressure on the joint, regular exercise is generally recommended, with swimming topping the list as gaining the most benefit with the least stress to the joints.
Treatment of Hip Dysplasia In many cases, simple restriction of exercise and perhaps aspirin as directed by the vet is all that the dog needs to remain comfortable. However, there are several options for the more severely affected dogs:
Non-traditional treatments (not validated by controlled trials):
Infectious Canine Hepatitis
(summarized From Carlson & Giffin)
This disease should NOT be confused with human hepatitis. This is a highly contagious disease transmissible only to dogs. It affects the liver, kidneys and lining of the blood vessels. It can sometimes be hard to distinguish from distemper as there are a variety of signs and symptoms that range from mild to fatal. Exposed dogs rapidly become contagious and remain contagious throughout convalescence.
Fatal form: the dog becomes ill, develops bloody diarrhea, collapses and dies. Puppies may die without symptoms.
Acute form: High fever, bloody diarrhea, possibly bloody vomit. Refusal to eat and painful movements. The dog can become light-sensitive.
Mild form: Lethargy, possible loss of appetite.
Interdigital cysts are a common problem in short haired breeds of dogs. Males do seem to be worse and Labs probably worst of all. There are a number of differential diagnoses to consider such as demodex, fungi, pyoderma secondary to atopy, dermoid cysts, etc. Dermoid cysts are invaginations of the skin which forms a pocket of hair and misc. junk. They are often infected and they always recurr unless surgically removed.
Especially if the cysts are recurrent, a good option is to have the cyst surgically removed and send it to a dermatopathologist, not a regular pathologist. It is expensive but it will greatly reduce the number of return trips to the vet. With that diagnosis, it will be easier to deal with future recurrences.
Other treatment includes long-term antibiotic treatment... three to six months may be required. Make sure the antibiotic choice and dosing is appropriate. Culture & antibiotic sensitivity tests are recommended.
Also demodectic mange may be underlying the problem. Skin scrapes can make the diagnosis, but false negatives are possible. Foot dips in mitoban (diluted) followed by warm soaks in dilute chlorihexidine may clear it up.
Fitting the dog with a rubber boot to protect the foot may help speed recovery following the removal of the cyst.
Kennel Cough (Infectious Tracheobronchitis)
This is characterized by a harsh, convulsive cough. It is persistent, contagious, and often develops into secondary complications, such as chronic bronchitis. This disease can eventually be fatal especially in the very young, very old, or already ill. If your dog is exposed to many other dogs, or will be boarded at a kennel, it should be vaccinated against this. It is so-called, because it spreads rapidly under "kennel" conditions -- many dogs kept relatively close together.
"Kennel Cough" is a generic name for a set of symptoms caused by a number of organisms. These include parainfluenza as well as bordatella, as well as many others. Dogs vaccinated with the bordatella vaccine can still get "kennel cough" because of all the bugs involved, but it tends to be much less severe. Bordatella vaccine is squirted into each nostril of the dog and should be repeated semi-annually. Parainfluenza vaccine should be a normal part of your dog's regular shots.
The vaccination is not effective for the first 24 hours, so if you are getting your dog vaccinated because you will be boarding it, get it done at least several days in advance!
Acute kidney failure, or kidney failure, is sudden and extreme and requires urgent care. Usually the dog recovers completely if it survives at all.
Chronic kidney failure, or kidney disease, is common in old dogs. The kidneys slowly wear out over a long time. It can be diagnosed by a blood test or urinalysis. Early signs include drinking and urinating more, since the kidneys need extra water, and foamy urine is sometimes seen.
Treatment is mostly dietary. They need a very low protein diet that is also low in certain minerals. The kidneys are stressed by too much protein and will wear out more slowly on a low protein diet. Dogs with sick kidneys should be given all the water they will drink.
The best known kidney diet is Hills K/D, but there is also Hi-Tor Neodiet, Neura Kidney Diet, and others. Some "senior dog food" is low in protein as well, but not as low as the kidney foods.
If you have any reason to suspect it, have the dog checked by a vet. Many old-dog kidney cases live happily for years with no special care other than the food.
Causes appear to be multiple. Trauma, such as excessive pulling on the leash or other pressure/force to the neck have been implicated. Older Labrador Retrievers account for a large proportion of cases. Overactive thyroid levels can contribute to the problem.
While the symptoms can vary somewhat, you will notice coughing while exhaling, particularly after exercise. The coughing sometimes sounds very odd. As the condition progresses, the dog may have problems breathing and panting. Secondary complications such as bronchitis, etc. may occur.
As there are various possible causes for shortness of breath and/or coughing, you must have your veterinarian look at the dog. The vet may put your dog under in order to examine the laryngeal muscles, xray to check the condition of the dog's lungs. Anesthesia is required to be able to observe the laryngeal muscles at work.
The standard treatment for dogs with LP is to surgically "tie back" one of the laryngeal muscles. This allows adequate air flow without giving pathogens, etc. completely unimpeded access to the dog's lungs. Typically, a specialist may be called in to do the surgery, it is not normally done in most veterinary clinics.
In most cases the disease is mild. Primary symptoms are fever, listlessness, loss of appetite and depression. Other symptoms involve the kidneys: a "hunched up" look due to kidney pain, ulcers on the mucus membranes of the mouth and tongue, thick brown coating on the tongue, bleeding from the mouth or bloody stools, severe thirst with increased urination. The whites of the eyes may turn yellow. Persistent vomiting and diarrhea are common. This disease is more prevalent in some areas than others. (Summarized From Carlson & Giffin.)
Many dogs seem to be allergic to the leptospirosis vaccination. If your dog is vaccination against lepto for the first time, keep a close eye on it for a few hours afterwards. If the dog goes into anaphylactic shock, get him back to the vet immediately.
Leptospirosis is a zoonotic disease, so if you come into contact with a dog that has Lepto, consult with your own doctor.
Obsessive Compulsive Disorder (OCD)
Retrievers that lick their paws excessively, horses that "stump suck", Dobermans that "flank suck" share the same disorder. The disorder is generally mild and most people never notice it, but sometimes it can go too far and become a hindrance to normal functioning.
Dr. Judith Rapaport (head of the Child Psychiatry Branch of the National Institute of Mental Health and author of "The Boy Who Couldn't Stop Washing") explored this area thoroughly, because of similarities with a human malady called "Obsessive Compulsive Disorder (OCD)." This is a disorder that induces unusual behavior such as an irresistible desire to wash your hands, over and over, even when they are not dirty.
The experiments at NIMH showed that this behavior is caused by a lack of Seratonin. This lack can be caused by a genetic predisposition and also by stress. Proper medication was shown to relieve similar problems in dogs, horses and people! Some of the reported results were on Labradors that literally licked the hair off of their paws, dropping the habit completely after medication.
This research is also a landmark in the understanding of the effect of some of the neural transmitters and has led to a whole new family of some wonderful new medicines. This work has already saved dogs, horses and people from one of nature's less pleasant maladies, and promises to shed light on other problems such as epilepsy.
The medication that Dr. Judith Rapoport found to work for dogs with acralick dermatitis as well as Obsessive Compulsive Disorder (OCD) is Clomipramine (brand name is Anafranil). However, Fluoxetine (brand name is Prozac) is now being used very successfully for OCD and has fewer side effects. You should discuss this with your vet, who will be able to prescribe these medications for your dog if it has OCD.
Some old-ish but very informative articles that describe this problem are "Chemistry of Compulsion" by Robert Trotter in the June 1990 issue of Discover magazine and the very thorough but easy to read article, "The Biology of Obsessions and Compulsions" by Dr. Rapoport in the March 1989 issue of Scientific American. Only the first article specifically mentions Rapoport's work with dogs, but if you want to understand what is really going on, read both articles.
Panosteitis (puppy limp)
Also called pano, this is an inflammation of the membrane covering the bone and is relatively common. Rest, quiet, and sometimes a vet-approved painkiller are generally recommended for the puppy. Some vets recommend a reduced protien (usually an adult mixture) diet. This can strike anytime between 6-18 months of age and rarely lasts past two years of age.
If the limping goes from leg to leg (i.e., one day the dog limps on the right rear leg and the next it limps on the left front), it is very likely pano. Pano can also be diagnosed via x-rays.
Fortunately, lasting effects are uncommon, and most puppies outgrow it. It is not known what causes pano, the belief is that there is either a hereditary link, perhaps just a predisposition toward, causing pano.
This is one of the most deadly viral infections for dogs. Young puppies who have not yet finished their vaccination schedules and dogs with compromised immune symptoms are most at risk.
Transmission & Symptoms
The virus is easily transmitted through a fecal-oral route. You can track in fecal matter on your shoes and expose your dog to it at home. Parks that have many dogs using it are high-risk areas, as are unknown dogs which may be shedding the virus. Some breeds, for example the Rottweiler, are more subsceptible to contracting this disease.
Lethargy and listlessness, proceeding rapidly to almost uncontrollable diarrhea and vomiting.
The puppy must be taken in immediately to the veterinarian for round the clock monitoring and IV's to replace the fluids the puppy is losing. If the puppy survives, he will make a full recovery. There are no lasting effects of the illness and he will be fully immune to the disease thereafter, assuming a healthy immune system.
A full series of vaccinations, with the last shot being scheduled for after 20 weeks of age is essential. Isolation -- don't let the at-risk dog be exposed to other dogs or their feces.
If you have an area (house and/or backyard) that has been exposed to a dog with Parvo, you can clean it up with a 3% bleach solution (3 parts bleach to 100 parts water).
There are many types and degrees of patellar luxation. The patella (kneecap) can luxate (dislocate) medially (towards the body midline) or laterally (away from the midline) and can be traumatic or congenital in origin. Small or toy breeds are much more likely to have this problem than larger breeds and they tend towards medial luxations; larger breeds tend to have lateral luxations if they develop this problem.
A system has been devised for grading patellar luxations:
Regarding surgical success, apparently about 50% of surgically treated cases demonstrate recurrent patellar luxation after 1-7 years although the severity of the patellar luxation at followup was reduced and about 90% (!) showed no signs of lameness. For the curious, the (incomplete) reference for these data is Willauer and Vasseur (1987) in Veterinary Surgery.
If you need to induce vomiting, first make sure that it's appropriate to do so.
Don't induce vomiting
National Animal Poison Control Center The National Animal Poison Control Center (NAPCC) provides a 24-hour emergency hotline that every dog owner should keep in plain sight. The hotline numbers are (800)548-2423 and (900)680-0000. The 800 number requires a credit card number and charges a flat $30; the 900 number is $2.95 per minute for a maximum of $30.
The NAPCC is a non-profit service of the University of Illinois and is the first animal-oriented poison center in the United States. Since 1978, it has provided advice to animal owners and conferred with veterinarians about poisoning exposures. The NAPCC's phones are answered by licensed veterinarians and board-certified veterinary toxicologists. They have specialized information that lets the experienced NAPCC staff make specific recommendations for your animals; plus over 250,000 records are in their database.
When you call, be ready to provide:
For further information, write to: The American Humane Association, 63 Inverness Drive East, Englewood, CO 80112-5117, or call (303) 792-9900.
Foods Chocolate, tea, coffee, cola:
It is not chocolate itself that is poisonous to dogs, it is the theobromine, a naturally occuring compound found in chocolate. Theobromine causes different reactions to different dogs: dogs with health problems, especially epilepsy, are more affected by theobromine than healthy dogs. Theobromine can trigger epileptic seizures in dogs prone to or at risk of epilepsy. The size of the dog will also be a major factor: the smaller the dog, the more affected it is by the same amount than a larger dog. Therefore, toxicity is described on a mg/Kg basis.
Furthermore, theobromine can cause cardiac irregularity, especially if the dog becomes excited. Cardiac arythmia can precipitate a myocardial infarct which can kill the dog.
Theobromine also irritates the GI tract and in some dogs can cause internal bleeding which in some cases kills them a day or so later.
Theobromine is also present in differing amounts in different kinds of chocolate. milk chocolate has 44-66 mg/oz, dark chocolate 450 mg/oz and baking/bitter chocolate or cocoa powder varies as much as 150-600 mg/oz. How much chocolate a dog can survive depends on its weight (and other unknown circumstances). Under 200 mg theobromine per kg body weight no deaths have been observed. Theobromine will stay in the bloodstream between 14 and 20 hours. It goes back into the bloodstream through the stomach lining and takes a long time for the liver to filter out.
Within two hours of ingestion, try inducing vomiting unless your dog is markedly stimulated, comatose, or has lost the gag reflex. If your dog has eaten a considerable amount of chocolate, or displays any of the above symptoms, take it to the vet without delay.
In the absence of major symptoms, administer activated charcoal. The unabsorbed theobromine will chemically bond to this and be eliminated in the feces. In pinch, burnt (as in thoroughly burnt, crumbling in hand) toast will do.
Walnuts are poisonous to dogs and should be avoided. In particular, there is a type of fungus common to walnuts (especially wet deadfall walnuts) that will cause severe episodes of seizuring. Many nuts are not good for dogs in general, their high phosporous content is said to possibly lead to bladder stones.
Onions, especially raw onions, have been shown to trigger hemolytic anemia in dogs. (Stephen J Ettinger, D.V.M and Edward C. Fieldman, D.V.M. 's book: Textbook of Veterinary Internal Medicine vol. 2 pg 1884.) Also: "Six Cases of Heinz Body Haemolytic Anaemia Induced by Onion and/or Garlic Ingestion" - CM Edwards and CJ Belford Aust.Vet.Prac. 26 (1) March 1996, 18-22.
Potato poisonings among people and dogs have occurred. Solanum alkaloids can be found in in green sprouts and green potato skins, which occurs when the tubers are exposed to sunlight during growth or after harvest. The relatively rare occurrence of actual poisoning is due to several factors: solanine is poorly absorbed; it is mostly hydrolyzed into less toxic solanidinel; and the metabolites are quickly eliminated. Note that cooked, mashed potatoes are fine for dogs, actually quite nutritious and digestible.
Turkey skin is currently thought to cause acute pancreatis in dogs.
Poisonous houseplants In assessing the risk to your dog from these plants, you need to consider both the age of your dog and it's propensity to chew on plants. Many of the below toxic plants rarely cause problems because most dogs don't chew them -- the exceptions being, of course, young puppies who are inclined to explore the world with their mouths, teething dogs who may chew on everything, and older dogs that are simply fond of chewing. Oleander, for example, is rather toxic, but most cases of poisoning involve 1) cattle, other grazing livestock 2) puppies and 3) human babies/toddlers.
Dumb cane is probably the one plant that should always be kept out of reach, since it takes only one nibble to have a potentially fatal situation.
(from Carlson & Giffin.)
That give rash after contact with the skin or mouth:
(mums might produce dermatitis)
Produce vomiting and diarrhea in some cases:
Puppy strangles occurs in puppies 4-16 weeks of age. It is a juvenile cellulitis of the face, ears, and lymph nodes. Affected puppies may have a fevero, be lethargic and not eat. The cause is unknown. An heritable immune dysfunction is suspected. CBC and biochemistry tests are normal in uncomplicated cases.
Bacterial cultures of lesions are negative except with secondary infection.
Biopsy results are multiple granulomas and pyogranulomas consisting of large epitheloid macrophages and neutrophils. Agressive therapy is indicated to prevent severe scarring of the face. Standard medications are usually steroids and antibiotics for secondary infections.
Rabies is probably the oldest and most well known (if also misunderstood) of the diseases that can affect almost all warm blooded mammals. Dogs are easily vaccinated against rabies: most counties and cities require that all dogs be vaccinated before they can get their dog licences, and veterinarians must report all the dogs they vaccinate. Thus it has one of the highest compliance rates of all the routine dog vaccinations available.
Rabies is transmitted by body fluids -- urine, saliva, or blood. Ironically, if your dog tangles with a rabid animal, you may be more at risk than your dog, since your dog is the one with regular rabies shots whereas these are rarely administered to humans.
For rabies to infect you, it must come in contact with the skin or be ingested. Dogs and cats can ingest it by getting the saliva or blood of a rabid animal in their mouths where it will be absorbed through the mucous membranes. Humans are particularly at risk since we have so many minute cuts in our skin, that if we touch our dog or cat after he/she has met a rabid animal, we can become infected.
Keep in mind that bites are the most common way for humans to contract rabies from dogs, although other routes are possible. Some other methods, such as urine spray from flying bats have been documented as a means of transmitting rabies, but you are unlikely to encounter dogs flying overhead.
Rabies cannot be detected by a blood test since it invades the neural system. The only detection at this time is by examining the brain after death for signs of the infection. The incubation time is 3-6 months, which is why the standard quarantine for animals in some countries is 6 months.
Call the local health inspector, animal control officer, or police if your dog or cat has tangled with another animal that you suspect might be rabid. Dogs and cats which have been vaccinated against rabies should wear a tag at all times when not in the house to prevent being destroyed to check for rabies. Most veterinarians will recommend another booster as soon as possible if the dog has been bit or is suspected to have been bit. The sooner the better to help protect against the virus before it has time to spread.
Despite the name, ringworm is caused by a fungus Microsporum canis and less frequently by other species. Ringworm infections remain limited to skin and superficial structures like hair and less frequently nails in cats and dogs. The infecting fungi require the keratin in superficial skin layers and nails, horns etc for their metabolism and furthermore do not grow well at the warmer temperatures of subcutaneous tissues, hence the superficial distribution. Note that ringoworm agents are obligate parasites - they normally live on the skin, although not in pathogenic numbers.
It can be transmitted between animals by skin abrasion or mild trauma, grooming tools, scabs etc particularly if the animal's immune system has been compromised, e.g. with steroids. In a normal, healthy animal ringworm infections are usually mild and self limiting, say 1-2 months. A major motivation for getting rid of a ringworm infection is to prevent you the owner from getting it.
If it is a mild infection topical application of lime sulfur is supposed to be good, although it can be smelly. Chlorhexidine shampoo is also effective as is also a relatively new 2% miconazole shampoo. If the infection is severe, oral griseofulvin is effective but expensive.
The round, ring-like lesions are suggestive but not diagnostic and are not even the typical lestion in cats and dogs. The animal may have itchy, scaly, crusty and hairless areas. Fungal culture is probably the best diagnostic method but many vets are not set up to culture fungi. A Wood's lamp can be used but not all ringworm agents will fluouresce so absence of fluourescence does not mean no ringworm, furthermore other things besides ringworm also fluoresce. In other words Wood's lamp is not a great test. Microscopic examination of skin scrapings may reveal the actual organism.
Finally, if you think your dog/cat has ringworm take it to the vet for diagnosis and treatment. If it does have ringworm, you can get it, but prevention is straightforward - treat your animal.
Common symptoms are:
In the March '92 issue of Dog World is an excellent article, "Autoimmune thyroid disease" by Dr. Jean Dodds DVM (a nationally recognized expert on the subject) explains a lot about thyroid conditions in dogs. She also goes to great effort to explain that dogs can be hypothyroid without showing the "classic" signs. She also explains typical course of treatment and followups. There's also a long list of breeds that are "predisposed" to problems.
Many vets do not take Dr. Dodds seriously because she does not publish in respected journals such as JAVMA but rather in "popular" magazines. So always discuss fully and candidly with your vet and bear in mind that many otherwise "asymptomatic" dogs are diagnosed with low or abnormal thyroid levels.
More subtle signs:
Padgett, George DVM "Canine Genetic Disease" Dog World, December 1996, January 1997, and March 1997 (in three parts). Bodner, E. "Hypothyroidism: a New Direction", AKC Gazette Feb 1997 , pp 40-42. Increasing attention is being paid to this problem. OFA now has a registry for thyroid function.
von Willebrand's Disease
Von Willebrand's disease (vWD) is an inherited bleeding disorder. It is a complex and difficult disorder to deal with, because genetics, diagnostic abnormalities, pathogenic mechanisms, and sometimes conflicting clinical signs are all involved. The commonality between all vWD is a reduction in the amount or function of von Willebrand factor (vWF), which is manifested through abnormal platelet function and prolonged bleeding time. Different breeds exhibit different variations of the disease, and some individual animals appear to "acquire" vWD.
While the bulk of the information available is based upon purebred dogs, the disease is not unknown in mixed breeds. The total number of breeds affected by vWF exceeds 50. The disease also appears in cats, pigs, horses, and humans.
Human variants of vWD are broken into three main types which can be used to describe canine vWD.
Type I vWD is characterized by a low concentration of normally structured protein. Breeds with a known prevalence of vWD in excess of 15% include Basset Hounds, Dachshunds (mini & std), German Wirehaired Pointers, German Shepherds, Keeshonds, Manchester Terriers (std & toy), Miniature Schnauzers, and Rottweilers.
Type II vWD is characterized by a low concentration of an abnormal vWF. Breeds in which severe type II-like vWD has been diagnosed include American Cocker Spaniels, German Shorthaired Pointers, and German Wirehaired Pointers.
Type III vWD is essentially the complete absence of vWF. Severe type III vWD has been diagnosed in Australian Cattle Dogs, Chesapeake Bay Retrievers, Fox Terriers (toy), German Shepherds, Scottish Terriers, and Shetland Sheepdogs.
In vWD dogs, bleeding can be spontaneous - usually from the mucosa of the mouth, nose, or gastro-intestinal tract. Injury that is accompanied by bleeding may continue unabated until a transfusion is administered. Whether or not bleeding from small wounds will stop without treatment is not predictable.
Living with one of these affected animals can get quite interesting. You must be careful with him in the house; by always having him on a leash or within our sight in a portable pen when outside; and by having a unit of frozen plasma at the veterinarian's at all times. Obviously, elective surgery is not advised. Required surgery can be preceded by transfusion with good results, though you can never be certain.
Lastly, most of these diseases can be stopped by testing before breeding, and through selective breeding. Unfortunately, experience and hearsay indicate that the AKC is not active in the enforcement of these preventive measures. Apparently the breeders, at least some of them, are not either. You should insist that the parents of a litter in a high risk breed have been checked prior to breeding -- and that the puppies have likewise been tested.
The "traditional" vWD test (non DNA based) has enormous problems with accuracy and determination of precise vWD status. The blood collection for the vWD test must be done very carefully: you can only extract blood once, and you must not shake or separate the blood. If the test is done consistently and very carefully it can be useful. However, it is difficult to diagnose vWD without the test as there are many other things that can cause a bleeding problem, such as warfarin (rat poison) poisoning. So you might see non vWD dogs bleeding to death that are kept in a rat infested environment, for example.
Homozygous dogs rarely survive puppyhood. Heterozygous dogs generally have clotting problems (taking longer to stop bleeding and form a scab) which generally show up when the dog's tail is docked, dew claws are removed, or other surgery is done in which the problem becomes apparent.
Wobblers -- Cervical Vertabral Instability
"Wobblers" is the common term for a spinal condition called cervical vertebral instability (also caudal cervical spondylomyelopathy). It has not been proven genetic, but it is widely considered to be as it is quite prevalent in the Doberman breed.
There are several different types, but in sum the neck vertabrae are unstable, which causes the vertabrae to move or causes the disks in between to swell. Some dogs have no pain but are paralyzed; other dogs are in extreme pain but are mobile and some dogs are both.
Not very much is known about this disease. The mode of inheritance is unknown (and it is only suspected to be inherited, not proven). There is no cure. As a stopgap, surgical or medical intervention to reduce the swelling or stabilize the vertebrae can be tried. There is no easy, safe method of diagnosis. The only method of diagnosis is by myelogram which in itself can paralyze or even kill the dog.
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