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Subject: rec.pets.dogs: Canine Medical Information [Part 1/2] FAQ
This article was archived around: 21 May 2006 04:22:20 GMT
Last-modified: 02 Mar 1998
There are many FAQ's available for this group. For a complete
listing of these, get the "Complete List of RPD FAQs". This article
is posted bimonthly in rec.pets.dogs, and is available via anonymous ftp
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in the body of the message.
This article is Copyright 1997 by the Author(s) listed below.
It may be freely distributed on the Internet in its entirety without
alteration provided that this copyright notice is not removed.
It may NOT reside at another website (use links, please) other
than the URL listed above without the permission of the Author(s).
This article may not be sold for profit nor incorporated in other
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without express or implied warranty.
Canine Medical Information, Part I
Cindy Tittle Moore, firstname.lastname@example.org
Table of Contents
* Addison's Disease
* Anal Sacs
+ 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
* Canine Parvovirus (CPV)
* Chondrodysplasia (CHD or Chd).
* Degenerative Joint Disease
* Elbow Dysplasia
+ Osteochondritis Dissecans
+ Fragmented Coronoid Process
+ Ununited Anconeal Process
+ Diagnosis and Registry
* Eye Problems
+ Retinal Dysplasia
+ Dealing with Blindness
* Gastric Dilation and Bloat
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
* 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 http://netvet.wustl.edu/.
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 email@example.com
with SUBSCRIBE VETMED yourfirstname yourlastname in the body of the
message. Be sure to substitute your own first and lastnames in the
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 (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
(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
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
* 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
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
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
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
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
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
firstname.lastname@example.org 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
(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
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.
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.
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
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:
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.
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,
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
_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
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
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
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 http://wrbu.si.edu/www/culicidae/heartworm.html.
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
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.
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
o Prevents hookworm infestations as well as heartworms.
o Safe for Collies. Monthly.
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, email@example.com