Questions cause of spinal cord compression in dog

We read with interest the recent “What Is Your Diagnosis?” article¹ involving an 8-year-old Japanese Chin with a history of chronic intermittent neck pain and acute tetraparesis. The cervical vertebral abnormalities described included occipitoatlantal malformation, a lack of a dens, and fusion of C2 and C3.

We agree that the spinal cord compression at the level of C1-2 is the most likely cause of the dog's clinical signs. We disagree, however, with the subsequent interpretation of the cause of this compression. The authors suggested that there is “[a] herniated disc at the intervertebral disc space of C1-2, causing extradural compression of the spinal cord …” and that there is “…spinal cord compression at the level of C1-2 secondary to intervertebral disk degeneration and herniation.” As far as we are aware, there is no intervertebral disk at C1-2, and embryologically, development of a disk at this space would not appear to be possible. Furthermore, this space should not be described as an intervertebral disk space because there is no disk at this location; the correct terminology would be intervertebral space. Thus, we disagree with the authors that the compression seen in this dog at the C1-2 space was a result of a degenerated and herniated disk. Importantly, the magnetic resonance images show a compressed triangular-shaped spinal cord and substantial dorsal cord compression. The more likely explanation of this compression is fibrous connective tissue hyperplasia with subsequent circumferential extradural compression resulting from chronic instability secondary to the absence of the dens. The hyperintensity noted on the T2-weighted images might also represent demyelination, edema, gliosis, or necrosis.

Of additional interest was the comment that “[g]iven the guarded prognosis and uncertainty of success with surgical management…,” the owners elected medical management. We do not quarrel with the guarded prognosis but take issue with the statement regarding the uncertainty of surgical treatment because C1-C2 stabilization, if performed correctly, directly addresses the dog's primary (and chronic) problem, the instability.

The authors suggested that medical management (rest and corticosteroids) resolved the clinical signs in this dog, but the dog was followed up for only 1 month. Because the primary problem of instability was not addressed, recurrent episodes are likely, if not guaranteed.

In sum, the authors stated this case represents “…the first report of a herniated disk at the intervertebral disk space at C1-2….” However, we question that conclusion. Rather than demonstrating the importance of “…diagnostic imaging in the diagnosis of a C1-2 disk herniation…,” we would suggest it better demonstrates the importance of knowing the anatomy of the vertebral column in dogs. Such an error also implies less than careful scrutiny during the review process. Lastly, we would propose a more comprehensive approach to management of atlantoaxial instability.

Randy J. Boudrieau, dvm, dacvs

Dominik Faissler, dr med vet

Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University, North Grafton, Mass.

The authors respond:

Thank you for your critical evaluation of our “What is Your Diagnosis?” article.¹ We greatly appreciate your efforts and desire to share your opinions on this particular case. Given the intricacies of the malformation (occipito-atlantoaxial [OAA] complex) we identified, our interpretation of the imaging studies and case management inevitably lead to conjecture.

Regarding our conclusion as to the existence of an intervertebral disk (IVD) herniation at the atlantoaxial (AA) articulation, we recognize the absence of an IVD at a normal AA articulation. Our intent was not to suggest that an IVD normally is present but instead hypothesize that through the abnormal development of the OAA articulation and, ostensibly, C3, an IVD developed between C1 and C2 and that ultimately, this abnormality developed into a degenerated and herniated IVD. If correct, then the term intervertebral disk space would be appropriate in defining the ventral AA articulation in this dog.

This dog had only six cervical vertebrae with fusion of the bodies of C2 and C3. From an embryologic basis, it appears there was a failure of centrum one to separate from intereentrum one, resulting in an enlarged ventral arch of C1 and an absence of a dens on C2; a remnant of the dens was evident on transverse computed tomographic images. We speculated that as a consequence of this maldevelopment, an IVD formed at the site where intercentrum two normally develops. This resulted in a kyphotic joint where the IVD and craniodorsal aspect of the body of C2 compressed the spinal cord. The development of a synchondrosis, rather than a synovial joint, presumably decreased the mobility of this joint.

We also recognize that alternate hypotheses may be as likely. We agree that a component of the spinal cord compression observed on the magnetic resonance images is a result of soft tissues associated with the abnormal AA articulation. Interestingly, dorsal plane T2-weighted images fail to disclose lateral compression, whereas dorsal compression remains. Unfortunately, dynamic imaging was not done to evaluate the degree of compression or laxity associated with the malformation. Given this, the viewpoint that surgical stabilization would address the dog's problems cannot be substantiated. Additionally, the paucity of evidence to support conservative versus surgical correction of typical AA subluxation, combined with the fact that our patient had minimal clinical signs, guided us to pursue conservative treatment, with the understanding that should deficits worsen, surgical intervention would likely be pursued. ^2,3 Per a telephone conversation, the dog was still doing well after 1 year. In the end, the speculative nature of our report remains as such.

Since publication of the report, we have had in-depth discussions with Drs. Alexander de Lahunta (Cornell University), Eric Glass (Red Bank Veterinary Hospital), and Marc Kent (University of Georgia) and gratefully acknowledge their expertise. Through interactions with these colleagues, we have gained further insight into this case.

Joan R. Coates, dvm, ms, dacvim

Stacey B. Leach, dvm

Jesse Nagy, dvm, ms, dacvr

University of Missouri, Columbia, Mo.

Eric N. Glass, ms, dvm, dacvim

Red Bank Veterinary Hospital, Tinton Falls, NJ.

Marc Kent, dvm, dacvim

University of Georgia, Athens, Ga.

Alexander de Lahunta, dvm, phd, dacvim, dacvp

Rye, NH.

The future of education for food animal practice

Within the past 10 years, food animal practice (FAP) has changed from individual animal medicine and surgery to population medicine. This has occurred in large part because of the change in status of farm animals from individuals to commodity groups (eg, fall calves). As a result, FAP, at least as it was practiced after World War II, has ceased to exist, except in regard to caring for food animals that could be considered ornamental (eg, purebred and hobby-farmed animals and animals with high financial or emotional value).

Increasingly, veterinarians are being asked to provide prophylactic and therapeutic protocols that can be followed and delivered on-site by animal health attendants, rather than hands-on diagnosis and treatment. This has led to the development of new skills (eg, competency with farm production software), but spending more time in an office means spending less time with the livestock, leading to more generic risk assessments rather than evaluations specific to a particular farm.

Not only are private FAPs no longer called on to attend to individual food animals, academic veterinary practices are not either. Whereas companion animals and horses still arrive at the doors of veterinary teaching hospitals, cattle, sheep, and pigs do not. Under the current model, therefore, veterinary teaching hospitals struggle to demonstrate farm animal syndromes and diseases as the demand for veterinary services such as examination, diagnosis, and case management falls.

Presently, few veterinary teaching hospitals have a viable FAP, and there is a paucity of food animal consultation practices that could serve as role models for interested students. Conventional pedagogical wisdom suggests that before a veterinarian can write a protocol for diagnosis and treatment of bovine respiratory disease in a feedyard, that individual must have first managed some individual cattle with pneumonia and have become familiar with the diagnostic support available to properly diagnose all aspects of the respiratory disease syndrome. In addition, he or she should have had an opportunity to examine health data from disease audit systems in feedyards to gain an understanding of the consultative model of FAP.

Without case material or consultation opportunities, teaching modern FAP becomes quite theoretical and learning modern FAP becomes appealing to only a small minority of students. By default, some veterinary schools will de-emphasize FAP because it is too expensive and too complicated to teach the small number of interested student participants. Eventually, we will be left without professors and instructors who are able to inspire sufficient clinical interest and acumen to be of any use to the livestock industries.

In response to this, teaching institutions may have to forsake the traditional model and create on-site clinical rotations, employing animal health attendants as teachers rather than veterinarians. Veterinary schools may have to pay for the learning opportunities involved in these rotations and may have to subsidize diagnostic support for FAP more than they do already. On the other hand, if FAP is taught exclusively through this consultative model, there is a risk of a two-class system of veterinary education, with equine and companion animal practice taught in the traditional way and FAP taught in a consultative way. As we consider the future of veterinary medical education, we must consider carefully whether this is the path we wish to take.

Eugene Janzen, dvm, mvs

Faculty of Veterinary Medicine, University of Calgary, Calgary, AB, Canada.

Balancing profit and animal welfare in swine production

I want to comment on the May 1, 2010, JAVMA News article “Protecting pigs, cultivating consumers.”¹ In that article, Dr. Paul R. DuBois' presentation at the 41st Annual Meeting of the American Association of Swine Veterinarians was summarized with the following: “Food production rules are being shaped on the basis of emotion, he said, citing as examples referendums and laws regarding confinement animal housing. Veterinarians need to base their arguments on science but must also provide a message with emotional impact, Dr. DuBois said. He said they need to be ready to phase out practices for which they cannot explain the benefits in emotional terms.”

Aren't we more sophisticated than ascribing emotion to obviously ethical concerns? Confinement housing of swine involves welfare concerns, and welfare is an ethical consideration. Is it right or wrong to house adult sows in gestational crates most of their adult lives? Does it violate their natures? I think few veterinarians would like to see pet dogs kept in such a manner, and swine are considered more intelligent than dogs and, therefore, more likely to suffer psychologically in such a system. I believe that confinement systems have reduced or eliminated many endemic swine diseases and improved survivability, thereby supporting profits. But confinement systems need to be examined for a balance between profit and animal welfare. I don't think the public will accept the production of cheap pork as the only goal in swine production, and the public passes the laws.

I recently was a guest during the presentation of class projects for a swine systems class at Colorado State University. Most of the students, in describing their ideal startup swine business, included the latest in confinement technologies, although there were concessions to animal welfare, such as outside exercise pens, in one case. Interestingly, of all the presentations, only one showed a paper profit, and this was by a student who mostly eschewed use of confinement practices for an extensive setup. Bill Niman of Niman Ranch has proved that extensive humane production of swine can be profitable. The bottom line is that there are things that can be done to maximize goals of animal health, welfare, and profit.

M. Lynne Kesel, dvm

Department of Animal Sciences, College of Agricultural Sciences, Colorado State University, Fort Collins, Colo.

Thoughts on feral cat control

As an epidemiologist, I dispute the comment by Dr. David Jessup reported in a recent JAVMA News article¹ regarding the human health impacts of feral cats. I believe he overestimates the public health risks associated with feral cats. Although trap-neuter-release is the common name for such programs, in truth they are trap-neuter-vaccinate-release (TNVR) programs. Sick cats are removed from the environment, and the proportion of healthy animals is increased so that the risk of disease transmission is lowered.

At the April 15, 2010, joint meeting of the California Conference of Local Health Officers Communicable Disease Control and Environmental Health Committees, Dr. Ben Sun, state public health veterinarian, stated the public health risk from feral cats is low. Dr. Sun noted that it is impossible to separate out the potential risks of exposure to the feces of feral cats from the risks of exposure to feces from pet cats and dogs. In fact, Dabritz et al² estimated that pet cats allowed to roam were responsible for 72% of outdoor fecal mass from cats. Furthermore, for cross-infection to occur, close contact with fecal material is necessary, such as by direct handling.

In addition, recent surveillance studies have found the prevalence of intestinal parasitism in cats is low. A study³ of fecal samples from 4 northern California shelters found the prevalences of Giardia spp and Cryptosporidium spp to be 9.8% and 4.7%, respectively. In New York State, a similar study⁴ also found the prevalences of these parasites to be low (7.3% and 3.8%, respectively).

And most importantly, recent genetic epidemiology studies have found that subspecies of Giardia and Cryptosporidium are host specific. Dogs and cats are commonly infected with Cryptosporidium canis and Cryptosporidium felis, whereas human infections are associated with Cryptosporidium parvum and Cryptosporidium homini. Similarly, genotyping data suggest transmission of giardiasis may be anthroponotic.^5–7

I agree with Dr. Jessup that TNVR alone is not the answer. However, trapping and removing cats has not been found to be effective. As long as the environment supports a certain population size, sexually intact females will continue to breed and other animals will move in. For example, before a TNVR program began at a colony near a hospital in Los Angeles County, there were as many as 300 cats. The hospital would trap and remove them every 6 months, and during each 6-month interval, the number of cats and kittens doubled or tripled. The current number of cats is now down to 52.

As long as more pets are born than can be adopted, there will always be abandoned animals, humanitarians who feed them, and compassionate veterinarians who discount their services. To achieve the goal of smaller, healthier colonies that do shrink over time, a coordinated effort is needed that supports TNVR programs, encourages pet adoptions, promotes spay and neuter laws, and discourages animal dumping. Most importantly from a public health perspective, pet owners and the general public must be made aware of the need for proper sanitation and good hygiene.

Deborah L. Ackerman, ms, phd

School of Public Health, University of California-Los Angeles, Los Angeles, Calif.; Oregon College of Oriental Medicine, Portland, Ore.