Health

French Bulldogs, although a fairly healthy and agile breed, have issues and care concerns that have been addressed by the following few articles and protocols, developed and shared with me by others who have been in the field of breeding and showing.

Spinal Health and Information about French Bulldogs

Degenerative and Compressive Structural Disorders (Last Updated: 29-Jan-2003)

K. G. Braund

Veterinary Neurological Consulting Services, Dadeville, Alabama, USA.

In this chapter we will review a variety of neurological disorders that result from abnormalities of

bones, ligaments, and other mesenchymal tissue that compress the nervous system. Most of

these conditions are degenerative in nature, although some represent developmental disorders.

The spinal cord and occasionally nerve roots are the nervous tissues most commonly

compressed. One condition, disk disease, represents the most common cause of spinal cord

compression in dogs.

An outline of this chapter is as follows:

Calcinosis Circumscripta/tumoral Calcinosis

Cervical Spondylomyelopathy

Disk Disease

Diskospondylitis

Dural Ossification

Lumbosacral Stenosis

Spinal Synovial Cysts

Spondylosis Deformans

Miscellaneous Disorders

Calcinosis Circumscripta/tumoral Calcinosis

Focal nodular aggregations of ectopic calcification occurring in the soft tissues have been

referred to by several synonyms that include calcinosis circumscripta, apocrine cystic calcinosis,

tumoral lipocalcinosis, lipocalcinosis, calcium gout and tumoral calcinosis. In man [1,2] the term

calcinosis circumscripta is used to distinguish between those generally smaller nodular calcareous

lesions occurring in the skin, subcutaneous sites and skeletal muscle and those histologically

similar but often larger multinodular lesions of tumoral calcinosis occurring in the deep

peri-articular sites, i.e. soft tissues located adjacent to joints. This nomenclature is beginning to

be more commonly accepted to describe similar distribution patterns of nodular deposits of

ectopic calcification in animals [3-5].

In the veterinary literature calcinosis circumscripta and tumoral calcinosis have been used as

synonyms to describe histologically similar idiopathic conditions characterized by the formation of

circumscribed single or multiple nodular masses due to deposition of calcinous material, located

either in periarticular connective tissue or in cutaneous tissues over pressure points and bony

prominences, in footpads, or in the mouth [6-11]. Etiology and pathogenesis remain obscure.

Most reports involve dogs, but the condition has occasionally been seen in cats [12]. Concurrent

illness is usually not associated with the different patterns of nodular ectopic mineralization in

animals; however, some animals may have underlying renal disease [4-6,13,14]. The prevalence

of the condition in young large-breed dogs, particularly German Shepherds, Great Danes and

Viszlas, suggests possible hereditary predilection. Calcinosis circumscripta has occasionally been

seen following surgical procedures, use of polydioxanone suture material, and progestin

(medroxyprogesterone acetate) injections in dogs and cats [15-19]. Calcinosis circumscripta-like

lesions have also been reported in dogs associated with the use of choke chains [20]. The

pattern of deposition referred to as tumoral calcinosis usually does not directly involve bones or

joints [4,8,11]. Clinical signs include one or more hard or fluctuant, spherical, well-circumscribed,

non-painful subcutaneous masses [8]. When incised, the masses discharge a chalk-like material.

Histopathologically, the masses are characterized by lobular areas of mineralization and

degeneration in a fibrous, collagenous matrix with large foamy macrophages, giant cells,

lymphocytes, and neutrophils. Some calcific foci are embedded by osseous tissue [4,8]. The

mineralized material stains positively for calcium, phosphorus, carbonates and hydroxyapatite

crystals. The ground substance stains positive for acid mucopolysaccharides

(glycosaminoglycans). The crystalline structures can be identified using scanning electron

microscopy [21]. The heterotopic ossification seen in a 7 year old German Shepherd with

fibrodysplasia ossificans may have resulted from the metaplastic change of calcinosis

circumscripta lesions [22]. In this dog, several mineralized densities were seen radiographically

ventrolateral to the lateral processes of the 6th cervical vertebra.

There have been several reports of calcinosis circumscripta/tumoral calcinosis (CC-TC) causing

spinal cord compression in young dogs (usually less than 1 year of age) in several breeds

including Bernese Mountain dog, German Shepherd, English Springer Spaniel, Rottweiler, and

Great Dane [23-26]. With the exception of upper thoracic cord compression (T2 - T3) in two

littermate German Shepherd puppies [25], all CC-TC masses resulting in spinal cord compression

have been localized at the atlantoaxial articulation [23,24,26,27], often in the area of atlantoaxial

ligament. The focal calcified masses are usually found lying over the spinal cord in the space

between the caudal aspect of the dorsal arch of the atlas and the cranial edge of the spinous

process of the axis, and extending into the vertebral canal. In the report involving the two young

German Shepherd littermates [25], a solitary mineralized mass was found on the dorsal laminae

between the dorsal spines of T2 and T3 and impinged ventrally on the intervertebral foramina.

The mass projected above the articular facets between the dorsal spinous processes.

Hematological and biochemical analysis of blood samples from affected animals are within normal

limits, as is cerebrospinal fluid (CSF) evaluation. Clinical signs of CC-TC will reflect either a cervical

syndrome or a thoracolumbar syndrome. Myelography will confirm spinal cord compression

associated with these masses. Special imaging, such as computed tomography and computed

tomographic myelography , may provide additional information on the extent of the mass and on

the degree of spinal cord compression [26]. In the cases of CC-TC reported to date with spinal

cord compression, the initiating mineralized mass lesion was the only lesion observed

radiographically. There has been a report of unilateral and bilateral mineralized masses

associated with the deep tendinous attachments on the lateral processes of the caudal cervical

vertebrae [28]. In this report, the masses occurred in three related Great Dane puppies (around 5

to 6 months of age) but were non-clinical and only of cosmetic significance. Surgical removal of

CT-TC masses in dogs with spinal cord compression is the treatment of choice and prognosis is

favorable.

Reports of solitary cartilaginous exostoses in three young, large breed dogs (Rottweiler, Bernese

Mountain dog, and St. Bernard), from 3.5 to 5 months of age [29], as well as in a 3.5 year old

Bernese Mountain dog [30], may actually be further examples of CC-TC, or, at least variants. In

each case, solitary, partially calcified lesions were localized to the atlantoaxial articulation and

caused tetraparesis from spinal cord compression. The radiographic features appear identical to

those described for CC-TC, including thickening of the dorsal arch of the atlas and malformation

and shortening of the spinous process of the axis [23,26,29,30]. The histopathological features

of the masses, however, appear to be different from those reported in CC-TC [5]. Surgical

removal of the mass was successfully achieved in the older dog [30].

Note: I thank Dr. Roy Pool, Mississippi State University, for his valuable comments on this

condition.

Cervical Spondylomyelopathy

Cervical spondylomyelopathy is a neurological disorder affecting Doberman Pinschers, Great

Danes and other large and medium-sized breeds in which abnormalities of the cervical spine

cause compression of the spinal cord [31]. Synonyms include wobbler syndrome, cervical

malformation-malarticulation, cervical vertebral instability, cervical vertebral malformation, vertebral

subluxation, cervical spondylolisthesis, cervical stenosis, caudal cervical spondylomyelopathy,

and cervical spondylopathy. Approximately 80% of cases occur in Great Dane and Doberman

Pinscher dogs and lesions are generally confined to the caudal cervical spine (i.e., C5 to C7).

The age of onset of clinical signs is variable, ranging from 3 months to 9 years. In general, Great

Danes are affected less than 2 years of age, while Doberman Pinschers more frequently manifest

signs when 2 years of age or older, with a clinical incidence peak between 4 and 8 years [32-34].

Several reports suggest male dogs are more commonly affected [35,36], although no gender

predilection was revealed in one study involving 170 dogs [32]. Cervical spondylomyelopathy

appears to involve both bony, fibrocartilaginous, and ligamentous abnormalities of the caudal

cervical spine.

These include:

Chronic degenerative 

a. disk disease,

Congenital bony malformation (stenosis of the vertebral canal and abnormal articulation of

the articular facets)

b. Vertebral instability or "tipping",

"Hourglass" compression by the dorsal (ligamentum flavum) and ventral (dorsal longitudinal

ligament and dorsal annulus fibrosus) ligaments, and

c. Hypertrophy of the ligamentum flavum. These changes, occurring alone or in combination,

can result in caudal cervical spinal cord compression [32].

d. The cause of cervical spondylomyelopathy remains uncertain but it may be multifactorial. Some

authors consider the disease to be a developmental malformation-malarticulation disorder

[35,37,274]. Hereditary factors have been suggested [38,39]. A possible familial trait was

suggested for affected Dobermans in New Zealand [32]. Other reports failed to find support for a

genetic basis, although recognizing the problem was more prevalent in certain lines of

Dobermans [33,35]. Nutritional status has been implicated, including a hypercalorific diet and

calcium excess in rapidly growing dogs [40-42], yet cervical spondylomyelopathy does occur in

animals reared on a balanced diet [33]. The impact of conformation, such as longer neck and

heavier head in affected dogs [42] playing a biomechanical role in this disease, was not

confirmed in one study in which radiographic changes were independent of several body

dimensions measured [32]. Interestingly, there was a positive correlation between longer rump

length and increased risk of neurological disease in this study. Cervical trauma from use of a

choker chain was not found to influence the presence of the disease [32].

Clinical signs are related to the severity of spinal cord compression and therefore are variable in

nature and degree. Clinical signs usually are first noticed in pelvic limbs. Eventually, all four limbs

are affected, with signs often being more pronounced in the pelvic limbs. There is ambulatory

tetraparesis with the thoracic limbs moving in a short, choppy manner. The neck is often carried in

flexion. There may be varying degrees of atrophy of infraspinatus and supraspinatus muscles. An

affected animal can have difficulty rising from lateral recumbency or from a sitting position. The

digits may knuckle when the animal walks and nails are often worn excessively as a result of

scuffing and dragging. Most dogs have a conscious proprioceptive deficit and demonstrate a

wide-based stance. Sometimes pain may be elicited upon neck manipulation. Clinical signs tend

to be slowly progressive but can be abrupt in onset when external trauma is suspected as

playing a major precipitating role. A Horner's syndrome may be present, perhaps more often in

dogs with severely herniated intervertebral disks, especially at the C6 - C7 region [35].

Diagnosis is based on historical data, signalment, clinical data, and radiography. Most dogs have

the following radiographic abnormalities [43]:

a. Tipping of the craniodorsal aspect of the vertebral body into the spinal canal which may be

exaggerated by neck flexion;

Stenosis of the vertebral canal, especially at the cranial aspect of the vertebrae. Normal

and abnormal values for vertebral canal dimensions have been established [32,44,275];

b. Malformations of the vertebral 

c. bodies (see below);

d. Narrowed disk spaces, often with accompanying spondylosis deformans; and

Degenerative changes in the articular facets. These changes may be seen radiographically,

alone or in combination.

e. In adult dogs, the most important abnormalities seen using survey radiography are narrowed

intervertebral disk space, vertebral malalignment (e.g., tilting or subluxation), ventral spondylosis

deformans, and a misshapen vertebral body [31,35,45]. Vertebral tilting and coning of the

vertebral canal with stenosis of the cranial orifice is primarily recognized in dogs less than 1 year

of age [31,32]. Vertebral changes may be seen radiographically in puppies as early as 3 months

of age [32] and the observation of normal radiographic appearance of cervical vertebrae at 6

weeks of age in one of these puppies suggested the possibility of vertebral deformity occurring

between the ages of 6 and 12 weeks.

Many animals have more than one site of compression, which may not be apparent on survey

radiography. In one study, plain films were inaccurate in 18 of 45 dogs (40%) [46]. Therefore,

myelography is essential to establish an accurate diagnosis and prognosis, especially if surgery is

to be considered. Conventional myelography is considered the technique of choice for initial

evaluation of dogs with cervical spondylomyelopathy since it provides an image of the entire

cervical spine [47].

Furthermore, myelographic studies may reveal various types of extradural spinal cord

compression:

a. Dorsal compression associated with hypertrophied ligamentum flavum;

b. Ventral compression from a bulging/hypertrophied annulus fibrosus;

c. Lateral compression from malformation of articular facets;

Compression from a stenotic vertebral canal or vertebral instability associated with vertebral

tipping [43].

d. Some clinicians are advocates of stress radiography/myelography (i.e., use of flexion, extension,

or traction of the cervical vertebrae) in order to better define the nature of the compressive lesion

(dynamic versus static) and better define the subsequent treatment. The measurement of

"stepping" of the vertebral floor of cervical vertebrae when the neck is flexed has diagnostic

significance [33]. However, complications may follow stress radiography. Hyperflexion of the neck

may exacerbate cord compression caused by vertebral tipping and neck hyperextension may

aggravate cord compression by closing the dorsal aspect of the intervertebral disk space which

can force additional disk material (nucleus pulposus and/or annulus fibrosus) into the spinal

canal. Neck hyperextension may also worsen pre-existing compression from the ligamentum

flavum [43] (it remains to be proved whether or not the apparent increase in cervical

hyperextension in the Doberman Pinscher breed as a whole, between 1934 and 1972, has a

role in cervical spondylomyelopathy [47]). Conversely, with soft tissue lesions, traction on the

cervical spine will often reduce the degree of cord compression by stretching or flattening

redundant annulus fibrosus and ligamentous structures [31,46]. While non-contrast and

intravenous contrast-enhanced computed tomography appears to have little advantage over

conventional myelography in cervical spondylomyelopathy [47], other specialized imaging

techniques may also play an important diagnostic role, e.g., computed tomography-myelography

may provide more information than conventional myelography as to the exact nature and degree

of compression, particularly in cases of severe spinal cord atrophy [47].

Gross pathologic findings include stenosis of the rostral end of the involved vertebrae, unstable

vertebrae associated with flattened, expanded and elongated articular facets, and hyperplasia of

the dorsal annulus fibrosus and ligamentum flavum in young animals. The abnormal relationship

of one vertebra to another may result in static or dynamic cord compression. Similar changes

occur in older animals along with degenerative lesions affecting the articular facets including

osteophyte formation, sometimes with encroachment onto the spinal cord [48]. In older dogs, the

fibers of the dorsal annulus fibrosus of the intervertebral disk appear hypertrophic or hyperplastic

and may be partially or totally ruptured, with disk material extruded up beneath the dorsal

annulus, although herniated disk material into the vertebral canal is infrequent. The nucleus

pulposus may show degenerative changes and can be mineralized [35]. Disks at C5 - 6 and

C6 - 7 are most frequently affected [33,35,49]. In both young and older dogs, gross vertebral

deformity may be found, often involving C6 and/or C7 in Dobermans and Great Danes

[33,35,50]. The deformity can vary from rounding off of the cranioventral epiphysis to its total loss

producing a triangular wedge-shape. Redundant ligamentum flavum resulting in dorsal cord

compression is reported in Great Danes [46]. Similarly, the above-mentioned hourglass

compression by dorsal and ventral ligaments as well as joint capsule of the facets, is seen

principally in Great Danes [31]. In the spinal cord, varying degrees of compression and spinal

cord atrophy may be present. Degenerative changes characterized by white and gray matter

necrosis, neuronal loss, and cavitation may be seen at the site of spinal cord compression. At

this level, lesions may be seen in all funiculi. Wallerian-like degeneration of white matter is seen

above (e.g., ascending tracts in the dorsal funiculi and more superficial portions of dorsolateral

funiculi) and below (e.g., descending tracts in ventral and deeper portions of lateral funiculi ) the

compressive lesion [37]. Myelin degeneration is often more predominant than axonal

degeneration. Arachnoid fibrosis is not uncommon.

Prognosis for spontaneous recovery is poor. In mildly affected cases, conservative treatment may

sometimes be beneficial over a 4 to 6 week period. This includes strict confinement, neck brace

to immobilize the caudal cervical spine, and anti-inflammatory medication. However, long-term

conservative therapy tends to be palliative [49]. Marked improvement has been reported in many

cases following decompressive and/or stabilizing surgery.

A plethora of reports are available on surgical treatment that generally falls into three categories:

Dorsal laminectromy 

a. for bony compression,

Ventral slot decompression, which is especially useful for ventral soft tissue compressions

that are not traction-responsive (such as annular protrusions or nuclear extrusions), and

b. Distraction or ventral slot decompression for traction-responsive soft tissue compressions

[34,51-58]. Distraction may be achieved with vertebral body pins/screws and bone cement,

distraction rods, or intervertebral washers, often in association with bone grafts in order to

encourage vertebral fusion [31,52,59].

c. The choice of surgical technique will vary according to the location of spinal cord compression

(ventral, dorsal, or lateral), the nature of the compression (soft tissue or bony), and whether or

not the lesion is single or multiple: up to 30% of cases in mature Dobermans may have multiple

protrusions of the annulus fibrosus [34,53]. The most common lesions are ventrally located,

involve soft tissue, and tend to be traction-responsive [31,46]. All surgical procedures have a

high potential for morbidity and post-operative complications, which include infection, implant

failure, and additional disk protrusions ("domino effect") in disks adjacent to fused or immobilized

segments [49,53,60]. It has been reported that short-term success rates are high (approximately

80 per cent) after any of the surgical procedures, but there is a high rate of recurrence (around

20 per cent) [276]. Iatrogenic Horner’s syndrome has been reported associated with cervical

surgery, presumably due to traumatic stretching of preganglionic pathways in the thoracic

vagosympathetic trunk within the carotid sheath [61]. Furthermore, neurological signs may be

more pronounced the day following myelography in dogs with cervical spondylomyelopathy [62].

Non-ambulatory patients require special care and intensive nursing (see spinal trauma) for

bladder control and prevention of urine scald and decubital ulcers. Physical therapy (see

rehabilitation) is extremely important to combat disuse and neurogenic muscle atrophy [49,63].

One suggested prognostic guide is as follows [64]:

1. Favorable - If there is one lesion and the dog is ambulatory upon presentation;

2. Guarded - If there is one lesion and the dog is non-ambulatory 

3. upon presentation;

Guarded to unfavorable - If there are two lesions and the dog is non-ambulatory upon

presentation.

4. The demonstration of spinal cord atrophy and/or pooling of contrast material within the spinal

cord in computed tomography-myelographic studies may also suggest a guarded to unfavorable

prognosis in dogs with cervical spondylomyelopathy [47].

Control measures might include identifying Dobermans with radiographic features of cranial canal

stenosis, vertebral tipping, and "stepping" of the cervical vertebrae once skeletal maturity has

been reached and removing them from any breeding program since these identifiable

abnormalities offer a reasonably accurate prognostication for future development of cervical

spondylomyelopathy in this breed [33]. Additionally, use of balanced rations without excessive

nutrition or mineral supplementation and perhaps neutering larger, faster-growing puppies might

be considered [33]. Cervical vertebral ratios may have potential as a breed-specific screening tool

for cervical vertebral instability [275].

There have been isolated reports of a similar wobbler syndrome in other canine breeds including

Rhodesian Ridgeback, Old English Sheepdog, Weimaraner, German Shepherd, Chow Chow,

Rottweiler, Pyrenean Mountain Dog, Golden Retriever, Labrador Retriever, Boxer, Irish

Wolfhound, St. Bernard, Airedale Terrier, Bernese Mountain Dog, Bull Mastiff, English Setter,

Irish Deerhound, and Old English Mastiff. In these breeds, the predominant sites of cord

compression were C2 - C3 and/or C3 - C4 [35]. A possible hereditary malformation of C2 - C3

vertebrae occurs in Basset Hounds less than 8 months of age [65]. Involvement of the C2 - C3

articulation has been noted in Beagles [35].

The wobbler condition has also been reported in older female Borzoi dogs (from 5 to 8 years)

[66]. The condition is believed to have a recessive mode of inheritance. The C6 - C7 articulation

was always involved in a spectrum of abnormalities that included vertebral instability, vertebral

luxation, intervertebral disk herniation, and spinal cord compression.

Disk Disease

Spinal cord compression secondary to intervertebral disk protrusion-extrusion continues to be

one of the most common neurological disorders seen in clinical practice [67]. Terms used for this

disorder include ruptured disk, prolapsed disk, slipped disk and herniated disk. Disk

protrusion-extrusion more accurately describes this process. Protrusion implies that the disk is

bulging into the vertebral canal as a result of dorsal shifting of central nuclear material. The outer

fibrous envelope of the disk is still intact. Disk extrusion indicates that the outer fibrous layers

have ruptured with subsequent extrusion of nuclear material into the vertebral canal. The clinical

expression of disk extrusion is referred to as disk disease. The term intervertebral disk

displacement is presently in vogue as another descriptor of disk disease.

There are 26 intervertebral disks in the canine and feline spinal column, excluding the coccygeal

region, and they form approximately 18% of the length of the spine. Disks are widest in the

cervical and lumbar regions, and narrowest in the thoracic spine. Each disk consists of two

structurally different regions: (a) a central gelatinous area, the nucleus pulposus (NP), and (b) a

surrounding fibrous envelope, the annulus fibrosus (AF), which contains an inner, more

fibrocartilaginous matrix termed the "transitional zone" (TZ) [68-71]. The NP is oval-shaped and

eccentrically positioned between the middle and dorsal thirds of the disk. It is a highly specialized

tissue originating from the embryonic notochord. Throughout fetal life, the NP is the fastest

growing region of the disk, and in the neonate, it occupies a considerable area of the disk. The

AF is a fibrocartilaginous tissue consisting of bands of parallel fibrous bundles that run obliquely

between adjacent vertebrae. The ventral annulus is about twice as wide as the dorsal annulus.

Biochemically, the major macromolecular components of the canine disk include collagenous and

non-collagenous protein (NCP), proteoglycan (PG) aggregates, and glycoproteins. The PG

subunits consist of glycosaminoglycans (GAGs) covalently bound to a central protein core. The

main GAGs in canine intervertebral disks are hyaluronic acid, chondroitin sulfate-4, chondroitin

sulfate-6, and keratan sulfate. Higher orders of aggregation intimately involve hyaluronic acid.

Aggregated PGs are formed by the association of many PG molecules with a single chain of

hyaluronic acid, the complex being stabilized by a glycoprotein link. The GAGs are long-chained,

sulfated polyanions that attach to the central protein core like the bristles of a brush.The greatest

concentration of the GAGs in disk occur in NP and TZ regions of the disk.

Structures that are anatomically and physiologically closely related to disks include cartilaginous

end-plates, vertebral end-plates, and conjugal and dorsal longitudinal ligaments. Conjugal

ligaments, also known as transverse intercapital ligaments, are present between the second and

tenth thoracic vertebral bodies in dogs, and between the second and ninth thoracic vertebral

bodies in cats. Conjugal ligaments run over the dorsal part of the disk, ventral to the dorsal

longitudinal ligament (a flat structure that lines the floor of the vertebral canal), and connect the

heads of each set of ribs. The conjugal ligaments play an important role in the prevention of disk

extrusion into the vertebral canal in the thoracic region. Dorsal longitudinal ligaments run the

length of the vertebral canal, are attached to the dorsal borders of the vertebral bodies and form

fan-like coverings over the dorsal aspects of each disk. Stretch of this ligament is thought to

partially account for pain associated with disk protrusion-extrusion. Cartilaginous end-plates are

thin layers of hyaline cartilage that cover vertebral body epiphyses and form the rostral and

caudal boundaries of each disk. Vertebrae on either side of the disk have a specialized plate of

dense, smooth bone termed the vertebral end-plate. These plates are perforated by numerous

small canals that are related to the underlying marrow spaces. Each plate consists of an outer

peripheral zone and an inner zone that accommodates the NP region of the disk.

Intervertebral disks function as very effective shock absorbers of the vertebral column, largely

due to the gel-like properties of the central NP. Specialized PGs within the nucleus bind many

water molecules to form a fluid system that is virtually incompressible. This hydrophilic property

allows the nucleus to deform and dissipate forces equally over the AF and cartilaginous

end-plates. The transformation of an axial compressive force applied to the spine into tangential

stresses on the annulus is the function of the NP, thereby reducing the compressive force on the

annulus itself. Disks also provide support for the spinal column, since they represent

amphiarthrodial joints in intervertebral articulations.

After birth, the canine disk undergoes structural changes that are most prominent in the NP

[71-73]. The gel-like nucleus is eventually replaced by more mature fibrocartilage. This process

occurs gradually in most breeds of dogs, so that by 7 to 8 years of age, the entire nucleus has

changed, and the distinction between nucleus and annulus is lost. In several other breeds of

dogs, however, the aging pattern is quite different. These breeds have been designated

chondrodystrophoid due to their characteristic endochondral ossification and intervertebral disk

morphology, and include Dachshunds, Beagles, Pekingese, French Bulldogs, Basset Hounds,

Welsh Corgis and Cocker Spaniels [70,71]. Such breeds are characterized by varying degrees of

short-limbed dwarfism. Other breeds such as Shih-tzus and Lhasa apsos probably should also be

included in this group. In chondrodystrophoid breeds, replacement of notochordal cells and the

gelatinous NP occurs as early as 4 months of age. This process is generally complete in all disks

by 12 to 18 months of age. The central areas of the NP are usually the last to be affected, and

extensive degenerative changes frequently precede the final chondrification of this area. With

increasing age, degenerative changes observed in the NP include matrix disintegration,

peripheral/central calcification, and localized areas of cell death. Radial fissures and clefts may

appear in the AF. Commensurate with the morphologic transmutation of the NP, collagen levels

approach 30 - 40% dry weight within 6 - 12 months. Extraordinary changes in all other

biochemical parameters occur during the first 2 to 3 years [74-76]. In comparison with disks from

non-chondrodystrophoid animals of similar age, PG levels in NP are 40 - 50% lower, glycoprotein

and non-collagenous protein values are 30 - 40% lower, and chondroitin sulfate values are

30 - 50% lower. Also, during this period, keratan sulfate replaces chondroitin sulfate(s) as the

major GAG. The degree of hydration of disks likely decreases with reduction in GAG content, as

has been shown in people. Degenerated disks have a depressed imbibition index, which is a

measure of the water-binding capacity of the disk.

The etiology of intervertebral disk protrusion-extrusion remains elusive. It is hypothesized that

significant changes in morphology and biochemical parameters of the disk during the first 2 years

of life result in a reduction of the disk's shock absorbing mechanisms [68,69]. While still retaining

limited properties of incompressibility, the NP loses its ability to adequately deform and distribute

forces in a centrifugal manner. As a result, the AF is subjected to increased loading from axial

compression and lower tangential stress, which is disproportionately distributed in the disordered

disk. The mechanical failure of the NP ultimately results in disruption of AF fibers and subsequent

protrusion-extrusion. Results of biochemical studies suggest that the mechanical efficiency of

disks is compromised in chondrodystrophoid dogs by 2 to 3 years of age [74-76]. This time-frame

is consistent with the occurrence of clinical disease. Nevertheless, this theory does not explain

why clinical disk disease occurs with a relatively high frequency in some non-chondrodystrophoid

breeds, such as Miniature Poodles and mixed-breeds; nor does it elucidate why clinical disk

disease occurs infrequently in older dogs of any breed. Studies in dogs have shown that disk

metabolism in the NP is mainly anaerobic, the main route of nutrient supply into the NP is via the

endplate, and that diffusion of nutrients is the main mechanism of metabolite transport [77].

There is probably an optimal, but as yet undefined, range of vertebral stress that is needed to

promote and maintain nutritive requirements of disks. Half an hour of moderate exercise per day

has been shown to increase nutrient flow into canine disks [78]. In contrast, spinal fusion in the

dog results in significant biochemical changes in disks-metabolism is depressed in the

immobilized disks but increased in the disks adjacent to the fusion mass [79]. In addition, water

content and imbibition of water in NP and AF are significantly depressed in fused disks. That disk

displacement occurs with some frequency in disks adjacent to totally calcified disks may also

reflect an overstressed disk. Finally, it is conceivable that loss of PGs and mechanical failure of

the NP profoundly influence disk nutrition. Whether disk matrix changes are the cause or the

effect of nutritional diffusion impairment remains to be determined.

There is no evidence that external trauma plays a role in disk degeneration. A force of sufficient

magnitude to result in spinal fractures and/or luxations rarely produces traumatic disk

protrusion-extrusion. Nevertheless, trauma has been implicated in several large-breed,

non-chondrodystrophoid dogs in which tearing of the dural mater secondary to intervertebral disk

injury occurred during periods of vigorous running and or struggling [80]. Although trauma does

not appear to play a role in the initiation of disk degeneration per se, it may be a factor in the

precipitation of protrusion-extrusion once the normal mechanical efficiency of the disk is impaired.

It is not unusual for dogs with clinical disk disease to be presented with a history of spinal trauma

of variable degree, such as jumping or falling. Perhaps the most logical explanation for the

prevalence of disk disease in certain breeds of dogs is a genetic one. Earlier studies suggested

that genetic factors are involved in the accelerated aging patterns of disks in Beagles [81]. The

heightened susceptibility to disk disease in Dachshunds has been explained by a genetic model

that involves the cumulative effect of several genes, with no dominance or sex linkage, subject to

environmental modification [82]. In some families of Dachshunds, the prevalence of disk disease

was found to be 62%, compared with the estimated breed prevalence of 19%. %. Genetic

osteological factors probably play a role as well. For example, midsagittal and interpedicular

diameters of the cranial and caudal aspects of cervical vertebral foramina (C3 - C7) are reportedly

significantly larger in small breeds than in large breeds and Dachshunds, with seemingly potential

predisposition to cervical spinal cord compression [274]. There is no evidence that autoimmune

mechanisms are a factor in the pathogenesis of disk degeneration. The roles of inactivity and

obesity in disk disease have not been fully evaluated, although in one study, excess body weight

did not appear to be a predisposing factor in Cocker Spaniels with disk disease [83].

Neurological signs after extrusion of disk material are caused by impact injury [84], or mechanical

compression of the spinal cord [85], or both. While disk protrusion usually precedes extrusion,

protrusion or bulging of the disk dorsally into the vertebral canal without rupture of the AF is not

usually associated with clinical signs, with the possible exception of pain. This is exemplified in

dogs and cats over 7 years of age in which dorsal disk protrusion is relatively common but is

subclinical. The velocity with which the disk material extrudes into the canal appears to be more

important than the size of the mass. An explosive herniation results in far more severe damage

than a slow extrusion. With acute impact injuries, hemorrhage and attendant inflammatory

reaction may also contribute to epidural compression. Results of a quantitative radiographic study

[86] suggest that the lumbar epidural space in Dachshunds is less than that in German

Shepherds (a non-chondrodystrophoid breed) which implies that epidural masses of similar size

would cause more spinal cord compression and more severe neurological deficits in Dachshunds.

For a review of the pathophysiological events and biochemical cascade occurring with acute

trauma to the spinal cord see spinal cord trauma.

Most dogs with disk disease are between 3 and 7 years of age. Eighty-five percent of disk

extrusions in dogs occur in the thoracolumbar area and 15% are cervical. Approximately 80% of

thoracolumbar extrusions occur between T11 and L3, with less than 2% occurring in the terminal

lumbar region (L5 - S1). In one study of large-breed, non-chondrodystrophoid dogs with

thoracolumbar disk disease, the mean age was approximately 7 years, and 57 dogs (92%) had

Hansen type 1 disk disease, usually at the L1 - L2 site [87]. In this report, 58% of cases were

acute in onset. Disk extrusion normally does not occur between T2 and T10, probably because

of the presence of the conjugal ligament, although a Hansen type 1 disk extrusion has been

reported at the T1 - T2 level in a 7 year old Dachshund with acute neurological deficits to the

hind limbs following trauma [88]. Several studies indicate that the most common site in the

cervical region is C2 - 3 [89,90]; although results of one study (105 cases) indicated no

significant difference in prevalence of disk disease affecting the first four disk spaces (C2 - 3 to

C5 - 6) [91] (in this study, prevalence of disk disease at C7 - T1 was significantly less than that

involving the first 4 disk spaces).

Disk disease also occurs in cats but mainly as a subclinical event [89]. One study on clinically

normal cats showed that degenerative changes in disks increased with age, with dorsal

protrusions found in 30% of cats 6 to 10 years of age, in 50% of cats 11 to 14 years of age, and

in all cats 15 years of age and older [92]. In another report, type I disk protrusion in cats, again

as a subclincial condition, was encountered most commonly in upper cervical and L4 - L5 areas

[93]. Nevertheless, clinical signs of disk disease have been reported sporadically in cats [94-96].

In a recent study of disk disease in 10 cats, there was no breed or sex predilection and clinical

signs included back pain, difficulty ambulating, and incontinence [96]. All herniations occurred in

the thoracolumbar spine, with a peak incidence at the L4 - L5 disk space. Eight cats had a

Hansen type I protrusion.

The onset of clinical signs in dogs may be acute (minutes), subacute (hours), or chronic (several

days or weeks). These signs may be rapidly progressive, slowly progressive, or may remain static.

Clinical signs also may undergo remission, only to recur at a later date. Clinical signs in dogs with

recurrent attacks frequently are more severe than those seen at the initial episode. Recurrences

have often been considered to be the result of multiple extrusions at the same disk level [97,98].

However, in a recent study, 22 of 25 dogs had a second operation (> 4 weeks after the initial

surgery) at a site distinct from the initial lesion [99]. In this study, Dachshunds were at higher risk

for recurrences than other breeds.

The two most common neurological syndromes associated with disk disease are thoracolumbar

and cervical syndromes. With cervical disk disease, the majority of affected animals will have a

history of pain, with or without paresis [90], and frequently, spasms of cervical musculature.

Animals may assume a posture with the nose held close to the ground and the back arched. In

some dogs, one thoracic limb may be held in partial flexion, with reluctance to support weight or

walk on this limb. These animals frequently show considerable pain on manipulation of the head

and neck. This combination of signs is termed root signature, since it is believed to be associated

with nerve root entrapment near the intervertebral foramen as a result of lateral disk extrusion

[100]. A lumbosacral syndrome is uncommonly associated with disk disease. In some animals

with lumbosacral disk extrusion, one pelvic limb may be held in partial flexion or a repetitive

"stamping" motion may be observed. These animals frequently show considerable pain on

manipulation of the limb and lumbosacral spine. This combination of signs has also been termed

root signature and is believed to be associated with nerve root compression or entrapment by a

fragment of extruded disk material. In a small percentage of dogs, a multifocal syndrome may

develop as a result of an acute, explosive extrusion of disk material from a thoracolumbar disk

that produces hemorrhagic myelomalacia. With this irreversible disorder, an initial thoracolumbar

syndrome may be followed by a lumbosacral syndrome as the lesion descends the cord. As the

lesion also frequently ascends the cord, signs of thoracic limb rigidity give way to flaccidity and

areflexia followed by death due to respiratory paralysis.

A definitive diagnosis of disk disease requires radiographic confirmation of presence of a mass

lesion or, in absence of a mass lesion, evidence of characteristic changes in the disk-vertebral

articulations. Typical radiographic features of disk disease include narrowing of the disk space,

intervertebral foramen and articular facet at the site of the herniated disk, wedging of contiguous

vertebral bodies so that the dorsal part of the disk space appears narrower than the ventral part,

and presence of an opacified mass in the vertebral canal. In situ calcified disks, in the absence

of any other abnormality, are a common finding in chondrodystrophoid breeds of dogs and are of

little significance-it has been estimated that dystrophic calcification occurs in 20 to 77% of disks in

some chondrodystrophoid breeds within the first year or two of life [71,101-103], especially in

Dachshunds in whom calcification appears to be inherited [104,272]. Recent studies suggest

that exercise has a modulating effect on rate of occurrence of disk calcification in Dachshunds

(moderate exercise reduced the rate of occurrence of disk calcification) [105]. In some cases,

particularly in acute extrusions, plain radiographic findings may be minimal or equivocal and

myelographic studies will be necessary to define the extent and location of spinal cord

compression. In one study, accuracy for determining sites of intervertebral disk protrusion using

survey radiography was only in the 51 - 61% range [280]. The importance of accurate localization

of lesions is demonstrated by the presence of asymmetrical neurological signs contralateral to the

myelographic and surgical lesion in some dogs, especially those with Hansen type 1 extrusion

[106]. Contrast studies also are indicated when there is evidence of more than one disk lesion.

The most common myelographic change is narrowing and dorsal deviation of the ventral contrast

column at the level of disk protrusion/extrusion. If the disk extrusion is acute, spinal cord swelling

may result in complete blockage of contrast material at, or immediately rostral to the level of the

disk extrusion. Note that dogs with thoracolumbar or cervical disk disease that have clinical signs

of back or neck pain alone, without neurologic deficits, may have substantial compression of the

spinal cord [90,107]. Results of experimental studies suggest that high-dose contrast

enhancement (e.g., 0.3 mmol/kg of gadoteridol) might facilitate the detection of recurrent

herniated disk fragments [108]. While plain radiography and myelography have long been the

methods of choice for the diagnosis of disk disease, other non-invasive neuroimaging procedures

such as magnetic resonance imaging (MRI) [109] and computed tomography (CT) [110-112] may

be more accurate, technically easier, and safer (myelography may exacerbate clinical signs and

induce seizures). In one report, preoperative CT confirmation of the relationship between the

spinal cord and the protruded disk was used in planning the surgical approach in dogs with

cervical disk disease [113]. MRI is considered to give better information about the condition of

the intervertebral disk (e.g., the hydration status of the nucleus pulposus) than radiography

[114]. In fact, classification of degenerating intervertebral disks and identification of MR imaging

characteristics of each type have been reported in experimental studies in dogs [115].

Hemorrhage may also be identified using MRI [278]. Analysis of CSF, especially if sampled from

the lumbar subarachnoid space, may reveal markedly elevated protein levels and increased

numbers of mononuclear white blood cells [116]. These changes are more likely to be found in

dogs with severe and acute neurological signs. Recent studies have shown a significant increase

in lumbar CSF glutamate concentrations in both acute and chronic cord compression injuries

secondary to disk herniation in dogs [117].

Gross pathological findings occurring subsequent to disk disease usually depend on whether

disk protrusion-extrusion is partial or complete and whether it occurs acutely or gradually. While

many disks in older animals of any breed may protrude, it is uncommon to find more than one

extruded disk, even in animals that have had a history of multiple episodes. This suggests that

many recurrences are due to multiple extrusions from single disks (see below). In disk protrusion,

the AF may bulge dorsally into the vertebral canal, without rupturing. This is known as a Hansen

type 2 disk [71], and it appears as a small, round to dome-shaped bulging of the dorsal surface

of the disk. A Hansen type 1 disk [71] is characterized by rupture of the dorsal annulus, with

extrusion of degenerate NP into the vertebral canal around the spinal cord. In some instances,

the extruded nuclear material will be contained by the dorsal longitudinal ligament. Typically,

disks extrude in a dorsomedian, paramedian, or dorsolateral plane. In the cervical region, where

the vertebral canal/spinal cord ratio is larger than that of the thoracolumbar region, lateral and

intraforaminal extrusions may be more common than in other spinal regions, producing spinal root

rather than spinal cord compression. Rarely, disk material may herniate through the cartilaginous

end-plate into the vertebral body (resulting in an intravertebral herniation or Schmorl’s node)

[118], or into the spinal cord itself (intramedullary extrusion) [279].

The spinal cord may be swollen, indented, flattened, or atrophic. In chronic cases, a fibrous

adhesion may be evident between the extruded mass and the dura mater. In many instances of

Hansen type 1 disk extrusion, hemorrhage will be associated with the extruded disk material,

producing a soft, granular, salt and pepper consistency. In some cases, the volume of epidural

hemorrhage may exceed that of the extruded disk material. The extruded material may form a

circumscribed mass or may lie flattened around the sides of the dura mater. The extruded

material may have migrated one or two vertebral levels away from the site of the affected disk.

This form of extrusion is usually present in dogs with thoracolumbar disk disease. Since extruded

disks are not completely absorbed, single disks that may have had multiple extrusions are

recognized by their stratified appearance. The oldest component may be dark gray, hard, and

adherent to the dura. Subsequent laminations are lighter in color and more friable [97]. In chronic

disk disease with slow, progressive extrusion, the degenerate material frequently has a gritty

consistency and an opaque and cheesy appearance. This type of extrusion is more often

observed in dogs with cervical disk disease.

Microscopic changes in the spinal cord are dependent on the rate of disk extrusion and duration

of cord compression. Gradual or mild compression produces varying degrees of demyelination

and axonal degeneration. Sudden, massive extrusions often result in focal or multifocal

hemorrhage and necrosis in gray and white matter. Localized edema may result in pronounced

cord swelling and collapse of the subarachnoid space. Rarely, disk material will be present within

the cord parenchyma. In necrotic areas of the spinal cord, vessels and mesenchymal (connective

tissue) elements are usually preserved. Lipid macrophages are observed in those cases of a few

days duration. In more chronic cases, marked proliferation of astrocytes and microglial cells may

be a feature, especially in areas that border the necrotic zone, together with trabeculae of blood

vessels and connective tissue that cross the necrotic areas [84]. In longer standing lesions, the

gray matter often has a fenestrated appearance due to loss of neurons and fibers. Astrocytic

gliosis may result in marked sclerosis of the gray matter. An epidural inflammatory reaction

composed of neutrophils, red blood cells, fibroblasts, large mononuclear cells, occasional

multinucleate giant cells, chondrocytic-like cells, and fibrocartilaginous debris may be present.

Medical management usually is directed at animals with their first signs of disk disease. Mild

clinical signs often resolve after at least three weeks of confinement with outside activity limited to

leash exercise. Recurrences of clinical signs are common in this group of animals. Severe,

unremitting pain may be managed with prednisolone, 0.5 mg/kg, PO, bid, for 72 hours. Muscle

spasms may respond to muscle relaxants, e.g., methocarbamol (Robaxin), 20 mg/kg, PO, tid, for

7 to 10 days, or diazepam, 2 - 5 mg, PO, tid, for several days. High dose methylprednisolone

succinate should be considered in paraplegic/tetraplegic animals with acute spinal cord injury

(see spinal trauma). Acupuncture is considered another form of conservative treatment

[119-122]. The analgesic response to acupuncture is reportedly most effective in dogs showing

pain with or without mild paresis. Animals receiving this treatment should have restricted activity.

Surgical treatment is indicated in animal with clinical signs unresponsive to medical management,

recurrent and/or progressive clinical signs, or in animals that are paralyzed. The approaches most

widely used are dorsolateral hemilaminectomy / pediculectomy or dorsal laminectomy for

thoracolumbar diskdisease and ventral slot-decompression for cervical disk extrusions, although a

thoracolumbar lateral approach has its proponents [89,123-128]. In a recent study, significant

improvement in clinical results was seen in caudal cervical disk protrusions when additional

surgical distraction and stabilization were provided following ventral slot decompression [129].

Dorsal laminectomy has also been successfully performed in dogs (especially those < 15 kg) with

cervical disk disease [130].While some studies of thoracolumbar disk disease indicate that

removal of disk material using these techniques significantly improves the degree of

completeness of recovery [131], successful results have been reported using fenestration alone

[98,132-134]. Prophylactic fenestration [89] in addition to decompression remains somewhat

controversial [135] but is still performed by many surgeons in order to reduce the chance of

subsequent herniation involving other disks [136-138]. A variety of other surgical procedures

have been described, including percutaneous diskectomy [139], but their effectiveness await

large clinical trials. Although still not commonly employed for the treatment of disk disease,

chemonucleolysis (e.g., using collagenase or chymopapain injected directly into the disk) has its

exponents [140-143] and may be more effective than fenestration at removing nuclear material

from the disk [144]. Experimental autographic disk transplantation for potential use in humans

with chronic disk disease is in its infancy but initial surgical studies in dogs showed promise [145].

Potential treatment complications include cardiac dysfunction from manipulation of the

vagosympathetic trunk during cervical surgery, and vertebral luxation as a complication of the

ventral slot procedure, especially in mid to lower cervical vertebrae [146]. Furthermore, cervical

vertebral fusion may predispose adjacent disks to herniation [147]. Corticosteroid therapy (usually

associated with use of dexamethasone) may lead to gastrointestinal hemorrhage, ulceration,

colonic perforation and pancreatitis [148-150].

Complications may be kept to a minimum by administering corticosteroids for as short a time as

possible. Prophylactic use of intestinal protectants, e.g., bismuth subsalicylate (Pepto-Bismol®) in

conjunction with frequent administration (at least four times daily) of antacids, e.g., magnesium or

aluminum hydroxide, or H2 antagonists such as cimetidine (Tagamet®, at 20 mg/kg, PO, tid) also

may reduce the prevalence of gastrointestinal hemorrhage. Corticosteroids should be stopped

immediately, when gastrointestinal complications are noted. In a recent study in dogs with acute

degenerative disk disease treated by surgery and corticosteroid administration, both omeprazole

(a gastric acid pump inhibitor) and misoprostol (a synthetic prostaglandin E1 analog) were

ineffective in treating or preventing the further development of gastric mucosal lesions [150].

Paralyzed patients need to be maintained in a sanitary environment, with twice daily bladder

catheterization, frequent removal of soiled bedding, and use of foam rubber pads or water beds

to prevent development of decubital ulcers. In addition , active physiotherapy (see also spinal

trauma and chapter on rehabilitation) that includes assisted standing and walking exercises, and

supervised swimming for 15 minutes twice daily, is an integral part of the nursing care since it will

delay disuse muscle atrophy.

The following statements may be used as a general guide to assess prognosis:

Animals that are paretic or paralyzed but have normal pain sensation have a good

prognosis following medical and/or surgical management. Results of a recent surgical study

(using hemilaminectomy and fenestration) with an 86% success rate indicated that the rate

of onset of clinical signs significantly influenced the clinical outcome but not the length of

recovery time, while the duration of clinical signs did not seem to significantly affect the

outcome, but did affect the length of recovery time [281]. The presence of postoperative

voluntary motor function is also reported to be a favorable prognostic indicator for early

return to ambulation [282].

1. Animals that are paralyzed with loss of bladder control and with reduced pain sensation

have a guarded-to-favorable prognosis following surgical intervention (decompression

and/or fenestration).

2. Animals that are paralyzed with loss of bladder control and loss of pain sensation have a

guarded-to-unfavorable prognosis.

3. Dogs with absent deep pain perception that undergo surgery within 12 to 36 hours have a better

chance of recovery (more complete and over a shorter time-period) than those in which surgery is

delayed [100]. Evaluation of the degree of myelographic spinal cord swelling might also assist in

establishing a prognosis in severely affected animals [151]. As a caveat to prognostication,

several studies have shown that severity of spinal cord dysfunction, based on clinical signs, does

not necessarily predict outcome. In one recent report, 50% of dogs with loss of bladder control

and loss of deep pain sensation recovered completely or partially [152].

A functional scoring system for pelvic limb gait of dogs with acute thoracolumbar spinal cord

trauma (from spontaneously-occurring disk disease) has been developed to allow quantification

of recovery to be assessed and potentially facilitate evaluation of pharmacotherapeutic clinical

trials [153]. Spinal cord evoked potentials and somatosensory potentials may be useful in

localizing spinal cord lesions and assessing lesion severity [154,155]. Other evoked potentials

such as magnetically elicited transcranial motor evoked potentials may be sensitive indices of

severity of spinal cord lesions in dogs with disk disease but do not appear to be reliable

predictors of neurologic recovery [156]. In one report involving 10 cats with disk disease,

prognosis was adjudged to be most favorable in cats following surgical decompression [96].

Diskospondylitis

Diskospondylitis is intervertebral disk infection with concurrent osteomyelitis occurring in

contiguous vertebral bodies [157-169]. This disorder occurs in young to middle-aged adult dogs

(typically non-chondrodystrophoid) usually of the larger breeds. Male dogs outnumber females by

approximately 2:1. Diskospondylitis has also been reported in cats, albeit infrequently [170-174].

Diskospondylitis may occur following iatrogenic trauma of the vertebral column (e.g., disk

curettage), foreign body migration, paravertebral injection, extension from a body organ abscess,

or more commonly from blood-borne septic emboli that reach the avascular intervertebral disk via

the capillary networks in the vertebral end-plates [158-161,175,176]. The source of infection is

not established in most cases. Possible initiating sites include the genitourinary tract, skin,

gingiva, and infected heart valves. In one dog, epidural abscess and diskospondylitis developed

after administration of a lumbosacral epidural analgesic [177]. Diskospondylitis has also been

found in a Bernese Mountain dog with immune-mediated polyarthritis [178]. Bacterial infection is

the most common cause of diskospondylitis and coagulase positive Staphylococci (S. aureus or

S. intermedius) are the most frequent isolates. Other organisms identified include Brucella canis,

Nocardia, Streptococcus canis, Escherichia coli, Acaligenes sp, Micrococcus spp, Proteus sp,

Corynebacterium diphtheroides, Mycobacterium avium, Erysipelothrix tonsillarum and

Actinomyces viscosus. In a recent study, novel organisms incriminated in canine diskospondylitis

included Pseudomonas aeruginosa, Enterococcus faecalis and Staphylococcus epidermidis

[179]. Fungal organisms including Aspergillus terreus, Paecilomyces sp (e.g.,Paecilomyces

varioti), Penicillium sp, Chrysosporium sp, Pseudallescheria boydii, and Coccidioides immitis have

also been cultured [163,164,166,180,181]. In one retrospective study involving 135 dogs with

diskospondylitis, the prevalence of dogs with Brucella canis was approximately 10% and sexually

intact male dogs were at risk as were dogs from the southeastern United States [182].

Immunosuppression may predispose some breeds, such as German Shepherds, Airedale

Terriers, and Basset Hounds to bacterial or fungal infection and subsequent diskospondylitis

[181,183-185]. Respiratory or gastrointestinal portals of entry are suggested for animals with

aspergillosis. Curiously, the majority of reports of disseminated aspergillosis in dogs have involved

German Shepherds [181,186-188] with organisms localizing most frequently in kidneys, spleen,

and vertebrae. In one dog with diskospondylitis due to Aspergillus terreus, multiple granulomas

with fungal elements were also found in the subarachnoid space associated with the nerve roots

of the cauda equina [183]. Hypothyroidism does not appear to be a predisposing factor in the

development of diskospondylitis.

Clinical signs are variable according to vertebral involvement, ranging from subtle spinal

hyperesthesia and stiffness, to severe paresis/paralysis. In more than 80% of affected dogs,

spinal pain is observed [189]. Affected animals may manifest depression, anorexia, and pyrexia.

Often they are reluctant to exercise or jump. Heart murmurs can be detected on auscultation in

some animals. Pleural effusion associated with paecilomycosis was reported in one dog [284].

Spinal cord and/or nerve root compression may result from proliferation of inflammatory tissue

and exostosis, subarachnoid or epidural abscessation, vertebral pathological fractures,

intervertebral disk protrusion/herniation, or excessive vertebral instability [177,187,190,191].

Spinal cord myelitis may also occur by extension of infection through the meninges.

Radiographic abnormalities include a concentric area of lysis of adjacent vertebral end-plates

early in the disease process. More chronic lesions are characterized by varying degrees of bone

lysis and proliferation, vertebral sclerosis, shortening of vertebral bodies, narrowed intervertebral

disk spaces, and ventral osseous proliferation that may bridge the affected disk space. Extensive

destruction of a vertebra may result in its collapse. Diskospondylitis may be present in more than

one disk space and commonly occurs in one or more adjacent disk spaces. Common sites of

diskospondylitis are the caudal cervical area, midthoracic and thoracolumbar regions, and the

lumbosacral joint. In dogs with grass awn migration, reactive bony changes may be seen on

ventral and lateral surfaces of vertebrae L2 through L4 [189]. The nature and location of the

changes along the spine may help differentiate diskospondylitis from malignant bone disease

[192]. The severity of the radiographic changes do not necessarily correlate with the degree of

clinical involvement. Results of a recent multicenter, retrospective study evaluating contrast

radiographic findings (myelograms or epidurograms) in canine bacterial diskospondylitis revealed

that 15 of 27 cases (56%) showed some degree of spinal cord compression, although in the

majority (approximately 73%) soft tissue was the compressive mass and the median compression

for all cases was only 5% of the vertebral canal [193]. Vertebral subluxation was evident in 20%

of these dogs. Stress radiography has been recommended for further evaluating dogs with

vertebral instability [193]. Radiographic signs of the disease may not appear for several weeks

after the onset of clinical signs. Hence, a radiographically normal spine does not preclude the

diagnosis of diskospondylosis. Magnetic resonance imaging can be diagnostic prior to

development of definitive radiographic abnormalities [194]. MRI findings in affected dogs have

revealed increased T2 and decreased T1 signal intensity of the soft tissues ventral to vertebral

bodies, the end plates of the same vertebral bodies and the intervertebral disk [195].

Blood and urine cultures should be obtained before starting antibiotic therapy. Reports of

positive blood cultures range from 45% to 75% of affected dogs, while urine cultures can be

positive in up to 50% of dogs [189,196]. In one report, fungal hyphae were identified in urine

sediment from 6 dogs [181]. While serologic Brucella titers should be checked because of the

public health significance, positive blood cultures are reportedly lower in dogs with Brucella

canis-induced diskospondylitis [182]. Percutaneous aspiration of the infected vertebrae using

fluoroscopy is a very useful diagnostic aid. In one study, positive bacterial cultures were obtained

from 9 of 12 aspirated disk spaces including 2 dogs in which blood and urine cultures were

negative [197].

Prognosis is usually favorable with aggressive long-term antibiotic therapy (e.g., from 2 to 4

months) if neurological signs are mild and the vertebrae are stable [198,199]. As a rule of thumb,

until culture results are available, the organism should be assumed to be a Staphylococcus. The

cephalosporins have been effective in the majority of small animal cases, e.g., cephalexin, at 22

mg/kg, PO, tid or cefazolin 20 mg/kg IV, qid for up to 5 days initially, if animals have fever or

progressive neurological signs, followed by oral antibiotics. The following drugs have been

recommended for treating diskospondylitis caused by other organisms [189,200,201]:

Microorganism Antibiotics

beta-hemolytic

Streptococcus sp.

Amoxicillin  

Brucella canis

Enrofloxacin

Doxycycline

Gentamycin

 Actinomyces sp. Penicillin G  

For more on this subject see: Degenerative and Compressive Structural Disorders http://www.ivis.org/advances/Vite/braund17/chapter_frm.asp?LA=1

 

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