by Bobbie Kelley
Khan, a 4-month old Kuvasz
puppy from our first litter (1985), had been in his new home for one month.
I received a call from the concerned and anxious owner. The puppy, lethargic
for a couple of days, now wouldn't rise, exhibiting excruciating pain all
over. His hind legs had no strength. There was high fever, lack of appetite,
and diarrhea. The veterinarian, uncertain of the diagnosis at first, treated
Khan symptomatically for fever and pain, and prescribed a precautionary
antibiotic. A radiographic and blood work-up was ordered. Over the next several
months, the clinical signs would subside and flare up again episodically,
showing a recurring pattern. Each relapse was often more severe than the last.
The initial symptoms were so generic that proper diagnosis was difficult.
Within several weeks of the onset of symptoms, however, diagnosis was simplified
by the physical changes that occurred. Enlargement of the ends of the long
bones (appearing as swollen joints), weakened pasterns, splayed feet,
and stunting of the long bone growth were seen. The associated pain kept the
pup relatively inactive, and when movement was required, his gait was restricted
and mincing. Radiographs taken at this stage confirmed the problem: HYPERTROPHIC
OSTEODYSTROPHY (H.O.D.) (1).
HYPERTROPHIC OSTEODYSTROPHY IS
Perhaps no other juvenile orthopedic
disorder in dogs causes such intense pain. There is no known cure; one can
only attempt to ease the suffering with anti-inflammatory medications and
analgesics. Some puppies show gradual improvement over the course of several
months and eventually recover fully, although some permanent stunting or bowing
of the long bones may occur. Others get progressively worse and either succumb
or are euthanized. Other than providing supportive care, the owner is relatively
helpless, as the outcome of the disease seems independent of the treatment
(2,3,4,5). Time drags as the owner waits, day by day, to see if the puppy
will improve or worsen. Hopes soar as the pup seems to feel better, only
to plummet at the next relapse. Khan's suffering ended at six months
of age, when prolonged anorexia, dehydration, and fever caused by the HOD
claimed his life. As breeders, our nightmare was far from over. By then,
in Khan's litter of eleven puppies, two other confirmed (and one other
suspected) cases of H.O.D had been diagnosed.
THE CAUSE OF H.O.D. REMAINS UNKNOWN
The cause of H.O.D. remains unknown
(2,6,7). Hindered by a lack of research dollars available to study such
a rare disease, veterinary researchers are unable to agree on the cause of
H.O.D. A review of the scientific literature since the 1930's reveals that
the cause of H.O.D. may be one or perhaps a combination of the following:
genetics, nutrition, infection, trauma, autoimmune disease, hormone imbalance,
or reaction to vaccination (1,2,5,6,8). Among affected puppies, there is
little that can be pointed to as a common denominator.
Genetics Seen only occasionally
in the canine population, some breeds are more commonly afflicted with H.O.D.,
namely Great Danes, Boxers, Irish Setters, Weimaraners, and several other
large, fast-growing breeds (1,4,5,6). The disease is sporadic, usually affecting
only isolated puppies in a particular litter or line. However, there are reports
of family clusters, entire litters, or significant numbers of littermates
being affected (1,3). Some breeders have experienced consistently high percentages
of pups with H.O.D. in related litters, suggesting genetic influences. This
was the case in our own breeding program. Khan's dam produced two litters
before she was spayed; 3 of 11 pups (27%) from the first litter and 3 of
8 (38%) in the second litter had H.O.D. An unaffected litter-sister to Khan
was bred once, and 3 of 9 (33%) had HOD. By contrast, three unrelated bitches
of ours have produced 26 puppies, none affected, raised with similar nutrition
and management. These observations are suggestive of recessive genetic mechanisms.
Yet when researchers twice bred two littermate Great Danes that had H.O.D.
in puppyhood, two normal, unaffected litters were produced (8). Other breeders
produce only one or two isolated cases from years of repeat breedings and/or
line breedings of closely related individuals. These data raise questions
about the genetic mode or transmission. It is unknown whether complicated
genetic mechanisms result in a predisposition to the development of H.O.D.
in certain individuals (1,2,5).
Nutrition H.O.D. has occurred in
puppies oversupplemented with vitamins, minerals (calcium), protein, and
calories. It is well documented that overfeeding highly palatable diets
free-choice promotes bone growth abnormalities (1,2,6). But experimental
oversupplementation has not been shown to consistently reproduce H.O.D. in
test puppies (1). Litters of puppies all fed and supplemented in the same
way may have only one or two of the pups affected with H.O.D. Overnutrition
may be an exacerbating factor but is probably not a direct cause, as pups
in all nutritional states have been affected (1,2). Vitamin C deficiency
has also been postulated to cause H.O.D.; the radiographic appearance of
HOD in dogs is similar to human scurvy. But the studies are controversial
and inconclusive at best, and there is no substantiated evidence to support
Vitamin C deficiency as a cause of H.O.D. (1,6,7,9). Dogs synthesize their
own Vitamin C; however, it has been suggested that certain breeds of dogs
may be predisposed to faulty Vitamin C metabolism. Since puppies with H.O.D.
rarely improve with dietary correction or Vitamin C therapy, the association
between nutrition and H.O.D. is inconsistent (1,2,4,7).
Infected puppies with H.O.D. commonly
have high fever, diarrhea, and sometimes upper respiratory signs. There
is suppurative inflammation within the metaphyses of the long bones, and
often an elevated white blood cell count (1,7,8). The systemic clinical signs
and the bilaterally symmetric inflammatory response seen histologically has
led some investigators to look for an infectious agent as the culprit (1,5).
To date, no causative organism has been found in H.O.D.- afflicted dogs, and
attempts to transmit the disease from affected to unaffected dogs have been
unsuccessful (1,5). Yet, some human diseases act in the same way; congenital
syphilis in humans looks very similar radiographically to H.O.D. in puppies,
and the causative microorganism in syphilis disappears from tissue very early
in the course of the infection (1). More studies of infectious agents as a
cause of H.O.D. are warranted.
Various other theories on the cause
of H.O.D. have been suggested, and these include trauma (overuse, overexercise),
autoimmune disease, calciotropic hormone imbalance, and reaction to vaccination
(1,5,8). We have noticed in our own experience (in all but one case) that
the initial onset of symptoms occurred within 48 hours of the pup's final
distemper vaccination. Whether this is a correlation, or simply coincidental
with the typical age of onset of HOD (4 months of age), remains unknown.
TALLY OF AFFECTED KUVASZOK IS HIGH
Although as yet not considered
by breeders to be a predominant disease in Kuvaszok, the tally of owners and
breeders who have experienced the problem is surprisingly high. When one
looks at the number of Kuvaszok affected relative to the Kuvasz population,
and compares this with the occurrence of H.O.D. in the general dog population,
there appears to be a disproportionately high occurrence in our breed. Regardless
of the specific cause of HOD, there may be an underlying genetic predisposition
for an animal to demonstrate the disease, thus explaining why some breed lines
display the disease more often than others. Because of this possible heritability,
until the cause of H.O.D. is verified, it would be prudent to cull affected
lines from breeding, so that H.O.D does not become any more prevalent in
the breed than it is already.
BREEDERS MUST SHARE INFORMATION
There has been an unfortunate tendency
among breeders to minimize the problems encountered in their breeding programs,
and to be reluctant to discuss them objectively. But when puppies are dying
after a long-suffering illness, it is time to bury our egos. This is not
simply a mild juvenile orthopedic problem which the dog, or surgery, can
compensate for as in the case of the more commonly observed hip dysplasia
(H.D.) and osteochondrosis (O.C.D.). While H.D. and O.C.D. are certainly
problems of concern in our breed, they are normally not life-threatening.
Though H.O.D is usually referred to as self- limiting and rarely terminal,
five of the nine H.O.D-affected puppies we have produced (56%) have died
from H.O.D or its complications. Breeder apathy will not only impede research
efforts at understanding H.O.D, but because of the limited gene pool among
Kuvaszok, could result in the proliferation of affected and carrier animals.
In 1978, Dr. R. P. Wright, a veterinarian
and breeder of Irish Setters, attempted to collect information from setter
breeders and owners through their breed newsletter. Similarly, I attempted
to compile information following the 1992 publication of an earlier version
of this article in several Kuvasz newsletters. A team of veterinary researchers
at the University of Florida was ready to assist me with this effort, and
a private foundation had committed $30,000. We sought to compile information
and conduct studies of affected puppies, with the goal of determining the
cause, and thereby perhaps developing a treatment for H.O.D. Despite heart-wrenching
stories of gorgeous puppies of distinguished breeding being crippled or
dying from H.O.D., breeder and veterinary cooperation was minimal (5). I
was unable to maintain the interest of the University or the private foundation
with the paucity of data collected. Despite our disappointing progress in
understanding H.O.D., I maintain a personal file on H.O.D., and I invite
any of you with firsthand knowledge of H.O.D. to send me your case histories
and pedigrees. Maybe someday they will prove useful.
1. Bellah JR. Hypertrophic osteodystrophy.
In, Bojrab MJ, ed. Disease Mechanisms in Small Animal Surgery, WB Saunders,
Philadelphia, pp. 858-864, 1993.
2. Alexander JW. Hypertrophic Osteodystrophy.
Canine Practice 5:48-52, 1978.
3. Woodard JC. Canine hypertrophic
osteodystrophy, a study of the spontaneous disease in littermates. Vet Pathol
4. Bookbinder PF. Hypertrophic
osteodystrophy: cause unknown, cure still unknown. Interview in: Cornell University
Animal Health Newsletter 8:7, Dec. 1990.
5. Lanting FL. Hypertrophic osteodystrophy
(HOD). In, Lanting FL. Canine Hip Dysplasia and Other Orthopedic Problems.
Alpine Pubs., pp 183-195, 1981.
6. Sinibaldi KR. Hypertrophic osteodystrophy.
In, Bojrab MJ, ed. Pathophysiology in Small Animal Surgery, WB Saunders,
Philadelphia, pp. 670- 676, 1981.
7. LaCroix JA. Juvenile orthopedic
diseases. AKC Gazette, p. 62, Nov. 1980.
8. Bellah, JR. Personal communication,
9. Teare JA, Krook L, Kallfelz
FA, Hintz HF. Ascorbic acid deficiency and hypertrophic osteodystrophy in
the dog: a rebuttal. Cornell Vet 69:384-401, 1979.
Copyright c 1996, by Bobbie Kelley.
Copies may be made, provided proper attribution is given.