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rec.pets.dogs: Canine Medical Information [Part 1/2] FAQ

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Archive-name: dogs-faq/medical-info/part1
Last-modified: 02 Mar 1998

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This article is Copyright 1997 by the Author(s) listed below. 
It may be freely distributed on the Internet in its entirety without
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It may NOT reside at another website (use links, please) other
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                      Canine Medical Information, Part I

   Cindy Tittle Moore,
   Copyright 1996.
Table of Contents

     * Prologue
     * Addison's Disease
     * Anal Sacs
     * Anesthetics
          + Why is anesthesia used for OFA X-rays?
          + How dangerous is anesthesia?
          + What can I do to improve the odds?
     * Autoimmune Hemolytic Anemia (AIHA)
     * Breathing Disorders
     * Bloody Stools
     * Brucellosis
     * Canine Parvovirus (CPV)
     * Chondrodysplasia (CHD or Chd).
     * Coccidiosis
     * Deafness
     * Degenerative Joint Disease
     * Distemper
     * Elbow Dysplasia
          + Osteochondritis Dissecans
          + Fragmented Coronoid Process
          + Ununited Anconeal Process
          + Diagnosis and Registry
     * Epilepsy
     * Eye Problems
          + CEA
          + PRA
          + Glaucoma
          + Cataracts
          + Retinal Dysplasia
          + Dealing with Blindness
          + References
     * Gastric Dilation and Bloat
     * Giardia
     * Heartworms

   Much of the information found in this article is summarized from
   Carlson & Giffin. I would like to thank them for their informative and
   accessible information. Any mistakes made in the summaries are my
   responsibility and not Carlson & Giffin's. I believe that I am within
   copyright laws by using summarizations (no direct quoting, except for
   the toxic plants section), my own organization of the material, and
   precise acknowledgement where relevant. -Cindy Tittle Moore
   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:
     * Shearer, Tamara S. DVM. _Emergency First Aid for your Dog_ Ohio
       Distinctive Publishing, Inc., 4588 Kenny Road, Columbus, OH 43220.
     * McGinnis, Terri DVM. _The Well Dog Book_, second ed. 1992.
     * Miller, Harry. _The Common Sense Book of Puppy and Dog Care_.
       Bantam Books, Third Edition (revised) (1987). ISBN: 0-553-27789-8
     * White, Darlene, DVM. "Eliminating the Threats of Zoonoses," in Dog
       World, April 1992 (v77n4); a Maclean Hunter Publication, 29 N.
       Wacker Dr., Chicago IL 60606-3298.
     * Hampton, John K. Jr., PhD, and Suzanne Hampton, PhD. _Senior
       Years: Understanding your Dog's Aging Process_. Howell Book House.
       1993. ISBN: 0-87605-734-2.
     * _Nutrient Requirements of Dogs, Revised 1985_ [there may be a
       newer revisi on] Published by the National Academcy Press, 2101
       Constitution Ave. NW, Washington, DC 20418
     This is written by the Subcommittee on Dog Nutrition, Committee on
     Animal Nutrition, Board on Agriculture, National Research Council.
     It reads pretty well for something put out by a committee. Lots of
     references. Lots of tables of nutrient contents of various
     foodstuffs. Don't expect any discussions of what dog food is best!
     For the most part, consumers are left to figure this out for
     * _The Collins Guide to Dog Nutrition_, 2nd Ed., HOwell Book House
       1987. ISBN: 0876054181.
     * Hart BL. "Effects of neutering and spaying on the behavior of dogs
       and cats: Questions and answers about practical concerns," in
       JAVMA 1991;198:1204-1205.
     * Houpt KA, Coren B, Hintz et al. "Effects of sex and reproductive
       status on sucrose preference, food intake, and body weight of
       dogs," in JAVMA 1979; 174:1083-1085.
     * Johnson SD. "Questions and answers on the effects of surgically
       neutering dogs and cats," in JAVMA 1991;198:1206-1213.
     * Marrion, Ruth, DMV. "New Views on Neutering," in _Purebred
       Dogs/American Kennel Gazette_, April 1992 (pp50-54).
   There are also many sources of online information about general
   veterinary matters. The best place to start is Ken Boschert's NETVET
   site, at
   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
   with SUBSCRIBE VETMED yourfirstname yourlastname in the body of the
   message. Be sure to substitute your own first and lastnames in the
   subscribe command.
   You can also do research and article searchs at most University
   libraries: ask the librarian about the following services: Agricola,
   BIOSIS Previews, CAB Abstracts (produced by Commonwealth Agricultural
   Bureaux), Focus on Veterinary Science & Medicine (produced by the
   Institute for Scientific Information). MEDLINE indexes about 60-70
   veterinary journals and is a place to start, but is not as
   comprehensive as the above services. If the library does not have them
   separately, they are also available on the Dialog service, which most
   University libraries subscribe to.
Addison's Disease

   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.
Anal Sacs

   (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.

   Remember that this is not intended as complete information by any
   means. Your best source for that is from your veterinarian. Don't be
   afraid to ask questions. IVC had a great article on anesthesia.
  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.
          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.
          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
  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.
  Other anesthesia pages
Autoimmune Hemolytic Anemia (AIHA)

   This disease is only partially understood at this time. See also
   Symptoms include:
     * pale gums, possibly yellow in severe cases
     * yellow feces (from bile pigments)
     * red or orange-brown urine (but may look normal)
   Procedures to reverse this condition include various chemotherapies,
   steroids, cyclosporin, and blood transfusions. However, the only
   "tried and tested" treatment is corticosteroid therapy. Other
   cytotoxic drugs, like cyclosporin, cyclophosphamide, azathioprine and
   danazol are recommended by various people, generally because somebody
   else recommended them somewhere else. Their actual benefit seems
   uncertain. The general consensus is that cyclophosphamide is the best
   of these drugs to use.
   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.
Breathing Disorders

   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.
Bloody Stools

   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)
     * Diarrhea syndrome: Severe depression, loss of appetite, vomiting.
       Extreme pain. High fever follows with profuse diarrhea. No other
       disease comes close to matching the amount of diarrhea induced by
     * Cardiac syndrome: Affects the muscles of the heart, especially in
       puppies. Puppies stop nursing, cry and gasp for breath. Death can
       occur suddenly or after several days. Puppies that recover often
       develop chronic congestive heart failure that may kill them
       several months later.
   Dogs may have either or both syndromes. Treatment is difficult,
   requiring hospitalization; those who recover are immune. The quarters
   of an infected dog should be thoroughly sterilized; a solution of 1:30
   bleach and water is recommended. As with any use of bleach, make sure
   you do not mix it with ammonia, which results in mustard gas and can
   kill you and your dog. Be sure to rinse the bleach off thoroughly
   after application.
   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:

   Dog       1.75%
   Bitch     2.01%
   (1.75 + 2.01)/2 =
   puppies   1.88%

   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
   _The Complete Alaskan Malamute_ by Riddle and Seely covers this
   disease fairly well.

   (Adapted from email discussion with Ron Mandsager,
   Coccidiosis is caused by protazoal parasites of either Eimeria spp. or
   Isospora spp. Crowding, poor sanitation, or stress may facilitate its
   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.o
   There is a mailing list for owners of deaf dogs that can help you
   answer many of your questions (mail for information). In addition,
   you should look at their informative web site,
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

   "Elbow Dysplasia" is a general term that includes any of several
    1. Osteochondritis Dissecans (OCD)
    2. Fragmented Coronoid Process (FCP)
    3. Ununited Anconeal Process (UAP)
    4. Degenerative Joint Disease (DJD)
   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:
     Grade I--minimal bone change on the anconeal process
     Grade II--additional subchondral bone changes and/or osteophytes
     Grade III--well developed degenerative joint disease
  Because awareness of these conditions is relatively new, there haven't been
  nearly as many assessments for elbow dysplasia as for hip dysplasia.
  In their reports, OFA separates ratings into dogs and bitches. Here are some
  stats, for the breeds with more than 1000 evalustions:
     Rottweiler, 1042 bitches, 38.1% dysplastic--890 dogs, 47.9%
     GSD, 2940 bitches, 18.2% dysplastic--2156 dogs, 23.9% dysplastic
     Labs, 1398 bitches, 10.4% dysplastic--801 dogs, 15.2% dysplastic
  It isn't known why males are consistently higher in percent dysplastic. This
  pattern is true for all 16 breeds listed as having more than 75 evaluations
  Besides OFA, GDC will also evaluate and rate elbows.

  Please see the independent FAQ on Canine Epilepsy.
Eye Problems

  Following are short synopses of the most common forms of eye problems. CEACEA
  (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. PRAPRA (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. GlaucomaThis 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.
  Once the retina is damaged and the sight is gone the options are as follows:
     * Inject the eye with a fluid which kills the fluid producing cells
       in the eye, hence no further increase in pressure and no pain.
       This is not a guaranteed solution.
     * Diode laser cyclophotoablation
     * Remove the eye and sew the lids shut. Probably the most practical.
     * Remove the eye and replace it with a prosthetic (i.e., glass eye).
       There are potential problems with infection of the eye socket.
  CataractsCataracts are relatively common in dogs and most are hereditary. An
  ACVO-certified veterinarian can easily detect these cataracts. Haziness or
  cloudiness in the eyes in older animals is often _not_ cataracts. Hereditary
  cataracts can be found in many breeds of dogs and can be detected early in
  age, so all breeding stock should be screened for cataracts before being
  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. Retinal
  Dysplasia There are several types of Retinal Dysplasia:
   Retinal Dysplasia-complete
          Relatively rare, puppies are blind from birth and appears to be
          a simple autosomal recessive. Mostly reported in Europe. No
          skeletal abnormalities are associated with this form of RD.
   Retinal Dysplasia-folds
          This form of RD is called "retinal and vitreal dysplasia with
          skeletal abnormalities" or "dwarfism with retinal dysplasia".
          In this disease, three different ocular phenotypes are present
          (normal, localized retinal dysplasia (retinal folds), and
          complete retinal detachment) and two different skeletal
          phenotypes are present (normal or dwarf). This is an inherited
          condition, whose mode of transmission is as follows: Call N the
          normal gene and rd the gene for retinal dysplasia.
          + N x N normal eyes, normal skeleton
          + N x rd classic symptoms, retinal folds, normal skeleton
          + rd x rd dwarfism, eye problems/blindness, skeletal problems
          The gene acts as an autosomal recessive in regards to dwarfism,
          but acts as though it were dominant when only one parent passes
          on the gene to its offspring.
          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:
          + 1/4 normal
          + 1/2 afflicted carriers, can be identified in puppies
          + 1/4 dwarf
          that the ocular and skeletal defects are inherited together,
          and that the skeletal effects act as a recessive trait and the
          ocular effects act as an incomplete dominant trait. This
          implies that 1) any Labrador with any type of RD is a carrier
          for dwarfism, and 2) at least one of the two parents of puppies
          with RD is a carrier for dwarfism. Retinal folds _may disappear
          with age_, so an accurate evaluation for RD requires that
          puppies be evaluated, ideally between 8 and 10 weeks of age.
          In mild cases of retinal dysplasia, sight is probably not
          affected much, if at all. In severe cases, skeletal
          abnormalities are present.
  Dealing with Blindness
          Dogs that become blind rarely have all that much trouble with
          it. Unlike humans, sight is not a primary sense; dogs would be
          much more upset at losing their sense of smell. Most people
          with a blind dog find that dealing with blindness is not
          difficult nor traumatic for the dog.
          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
          For more information on Canine Eye disease contact:
     CERF (Canine Eye Registration Foundation)
     South Campus Courts C, Purdue University, West Lafayette, IN 47906
          Vanderlip, Sharon Lynn, DVM. _The Collie: A Veterinary
          Reference for the Professional Breeder_.
          Dr. Lionel Rubin, V.M.D., U of PA Vet Sch on Retinal Dysplasia.
          Carrig, Sponenberg, Schmidt, Tvedten, JAVMA, Nov 1988.
          Oliivero, DVM, Retriever Field Trial News, June 1993.
          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.
          Barnett, KC, et al: Hereditary retinal dysplasia in the
          Labrador Retriever in England and Sweden. J of Small An Prac,
          10:755, 1970.
          Carrig, CB, et al: Retinal dysplasia associated with skeletal
          abnormalities in Labrador Retrievers. JAVMA, 170:49, 1974.
          Carrig, CB, et al: Inheritance of associated ocular and
          skeletal dysplasia in Labrador Retrievers. JAVMA, 193:1269,
          Neslon, B, MacMillan, A.: Multifocal retinal dysplasia in the
          field trial Labrador Retriever. JAAHA, 19:388, 1983.
Gastric Dilation and Bloat

     Other references:
     _Note: Current thinking is that dogs with certain physical features
     (large, deep chest and high tuck) are most likely to bloat. The
     most recent research has not implicated diet -- although dogs that
     have previously bloated seem to benefit from carefully scheduled
     feeding._ The following information is several years old now.
          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.
          + The stomach is full of gas and begins to swell: gastric
          + The stomach partially rotates on its axis: torsion.
          + The stomach rotates 180 or more degrees: volvolus.
          Some facts (from Carlson & Giffin):
          + Dogs who bloat are almost always at least 2 years old.
          + Two-thirds are male.
          + Larger, deeper chested breeds are affected.
          + They eat large amounts of dry kibble.
          + They exercise vigorously after eating and tend to drink water
            in large amounts after meals.
          + They may have a history of digestive upsets.
          + There may be a familial association with other dogs who
          According to Carlson & Giffin, the symptoms are: excessive
          salivation and drooling, extreme restlessness, attempts to
          vomit and defecate, evidence of abdominal pain and abdominal
          distension. Abdominal fullness, whining, pacing, getting up and
          lying down, stretching, looking at the abdomen, anxiety.
          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") [From the Bloat Panel, sponsored by the Morris Animal
          Foundations, published in the August 1992 Irish Setter Club of
          America's _Memo To Members_.]
          + Feed two or three times daily. Be sure someone is around to
            observe after-feeding behavior for possible symptoms.
          + Water should be available at all times except immediately
            after feeding, especially if the dog seems to over-drink. Or
            mixing dry kibble and water before eating to prevent later
            swelling up in the abdomen.
          + Vigorous exercise, excitement and stress should be avoided
            one hour before and two hours after meals. Walking is alright
            and may help stimulate normal gastrointestinal function.
          + Any dietary changes should be introduced gradually over
            several days.
          There is another article about bloat in the Spring '92 issue of
          _Today's Breeder_ (published by Purina dog foods) (pp 8,9,15).
Giardia (prepared by Dr. James Coggins)

          If your dog has been diagnosed with Giardia, it is infected
          with the one-celled protozoan parasite Giardia lamblia. These
          flagellate parasites are usually contracted by drinking
          contaminated water or sometimes by eating contaminated feces.
          Giardiasis, the disease caused by Giardia, can range from
          asymptomatic (no visible signs of distress) to extremely acute
          where the dog is severely ill. Canine giardiasis should be
          treated since it is potentially transmissible to humans and
          other animals.
          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
          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.

          See also
          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 &
          The rest of the information on heartworms was adapted from a
          very informative post by Kristin Thommes who posted it March 5,
  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
          Can another dog can get heartworm by coming in contact with an
          infected dog's blood? (transfusion, bite)
     No. If a dog was infected and had circulating microfilaria, and
     these microfilariae were transplanted into a healthy dog via a
     transfusion, the healthy dog would NOT get adult heartworms because
     the lifecycle could not be completed within the body of the dog. A
     mosquito is needed for development from the L1 to the L3 stage.
          Could a pregnant bitch with heartworms give them to her own
     No, for the same reason as above, you need the mosquito for the
     intermediate stages between microfilarae and adult worms. While the
     placental barrier will keep the microfilarae out, even if this
     barrier broke down (which can happen), the pups will not be
          How do those medications work anyway?
     There are basically 2 types of medication available that will help
     to prevent adult heartworm formation in dogs that are negative. One
     type is the daily medication Diethlycarbamazine (DEC). It works by
     killing any larvae that have crawled into the dog from the mosquito
     within approximately the past 36 hours. DEC kills L3 larvae. Once
     they molt into L4's, DEC will not kill them and these larvae may
     develop into adult worms.
  Preventive Medications
          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
          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
     _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. I do not know how this functions or how it differs in
     treatment considerations for the dog. _
          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!
  Summary Of Medication
          Heartworm preventives include
          + Interceptor
               o Prevents hookworm infestations as well as heartworms.
               o Safe for Collies. Monthly.
          + Ivermectin
               o Excellent control of hookworms and roundworms as well as
               o Has caused seizures in higher doses to Collies. Monthly.
          + Filarbits Plus
               o Contraindicated if microfilariae are already present in
               o Controls hook, round, and whip worms to some extent. Can
                 be used in puppies 8 weeks or older. Daily.
    Canine Medical Information, Part I FAQ
    Cindy Tittle Moore,
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