Vertebral Hiperostrosis

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Vertebral Hyperostosis in Anteaters (Tamandua tetradactyla and Tamandua mexicana): Probable Hypervitaminosis A and/or D Author(s): Graham J. Crawshaw and Sergio E. Oyarzun Source: Journal of Zoo and Wildlife Medicine, Vol. 27, No. 2 (Jun., 1996), pp. 158-169 Published by: American Association of Zoo Veterinarians Stable URL: Accessed: 25/01/2010 08:53 Your use of the JSTOR archive indicates your acceptance of JSTOR's Terms and Conditions of Use, available at JSTOR's Terms and Conditions of Use provides, in part, that unless you have obtained prior permission, you may not download an entire issue of a journal or multiple copies of articles, and you may use content in the JSTOR archive only for your personal, non-commercial use. Please contact the publisher regarding any further use of this work. Publisher contact information may be obtained at Each copy of any part of a JSTOR transmission must contain the same copyright notice that appears on the screen or printed page of such transmission. JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact [email protected]. American Association of Zoo Veterinarians is collaborating with JSTOR to digitize, preserve and extend access to Journal of Zoo and Wildlife Medicine.

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Page 1: Vertebral Hiperostrosis

Vertebral Hyperostosis in Anteaters (Tamandua tetradactyla and Tamandua mexicana):Probable Hypervitaminosis A and/or DAuthor(s): Graham J. Crawshaw and Sergio E. OyarzunSource: Journal of Zoo and Wildlife Medicine, Vol. 27, No. 2 (Jun., 1996), pp. 158-169Published by: American Association of Zoo VeterinariansStable URL: 25/01/2010 08:53

Your use of the JSTOR archive indicates your acceptance of JSTOR's Terms and Conditions of Use, available at JSTOR's Terms and Conditions of Use provides, in part, that unlessyou have obtained prior permission, you may not download an entire issue of a journal or multiple copies of articles, and youmay use content in the JSTOR archive only for your personal, non-commercial use.

Please contact the publisher regarding any further use of this work. Publisher contact information may be obtained at

Each copy of any part of a JSTOR transmission must contain the same copyright notice that appears on the screen or printedpage of such transmission.

JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range ofcontent in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new formsof scholarship. For more information about JSTOR, please contact [email protected].

American Association of Zoo Veterinarians is collaborating with JSTOR to digitize, preserve and extend accessto Journal of Zoo and Wildlife Medicine.

Page 2: Vertebral Hiperostrosis

Journal of Zoo and Wildlife Medicine 27(2): 158-169, 1996

Copyright 1996 by American Association of Zoo Veterinarians


Graham J. Crawshaw, B.VeLMed., M.S., and Sergio E. Oyarzun, M.S.

Abstract: Hyperostosis of the thoracolumbar and coccygeal spine was seen in five captive ta

mand?as (Tamandu? tetradactyla and Tamandu? mexicana). Radiologie signs of the condition,

evident within the first year of captivity, progressed from a small subvertebral linear density to

massive vertebral hyperostosis and fusion. Clinical signs only developed in one tamandu? with

advanced hyperostosis. Soft tissue mineralization, observed during postmortem examination, is com

mon in tamand?as in other zoos. Plasma calcium levels were not significantly higher in captive tamand?as than in nine wild animals sampled. Plasma phosphorus, vitamin A, and vitamin D levels

were considered normal, but liver vitamin A levels were higher than levels in most normal domestic

animals. Vitamin levels in the diet were progressively reduced over 5 yr from a high of 57,000 IU/

kg vitamin A and 6,700 IU/kg vitamin D (dry matter basis) to 22,000 IU/kg and 1,900 IU/kg, respectively. Hyperostosis developed more slowly in animals fed diets containing the lower levels

of vitamins A and D, concentrations still considered excessive for this genus. The condition is most

likely caused by chronic hypervitaminoses A and/or D.

Key words: Anteater, Tamandu?, hyperostosis, spondylosis, hypervitaminosis.


Tamand?as (Tamandu? tetradactyla and

T. mexicana), are medium-sized arboreal

anteaters living in Central and South Amer

ica from Mexico to Paraguay.23 They have

been maintained in low numbers in captiv

ity for many years, but reproduction is un

common. Initial poor survivability in zoos

was likely related to their specialized di

etary requirements.9

The Metropolitan Toronto Zoo (MTZ)

acquired two female T. mexicana in 1981, and a male was received the following year. Each adjusted well to captivity and accept ed the diet offered. In 1987, the male de

veloped flaccid posterior paralysis and uri

nary retention. Radiography revealed exten

sive spondylosis and exostoses of the tho

racic, lumbar, and coccygeal vertebrae.

Minimal clinical improvement was seen

over the next few days, and the animal was

euthanized (animal 1). Survey radiographs of the two females (animals 2 and 3) re

vealed similar lesions in the axial skeleton,

although they showed no motor or other

neurologie deficits. One of these animals

(no. 2) died in 1989.

In December 1986, two additional ta

mand?as (T. tetradactyla), one male and

one female, were acquired. Both these new

er animals, normal when first examined,

also developed hyperostosis of the axial

skeleton (animals 4 and 5). Similar lesions

have been seen in tamand?as in other zoo

logical institutions (P. Wolff, Minnesota

Zoological Gardens; J. Ott-Joslin, Wood

land Park Zoo; J. Flanagan, Houston Zoo,

pers. comm.) and in the giant anteater (Myr

mecophaga tridactyla).

In this report, we describe the clinical,

radiographie, and pathologic findings in

these animals and the possible causes of

this condition.


All five tamand?as maintained at MTZ

were wild caught and were acquired from

commercial suppliers. Until 1985, the ani

mals were housed in a mixed-species public

exhibit, after which they were kept singly or

in pairs in hospital pens for breeding and

study purposes. Plasma calcium and phos

phorus levels from nine wild T. tetradactyla,

From the Metropolitan Toronto Zoo, 361A Old Finch

Avenue, Scarborough, Ontario M IB 5K7, Canada.


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captured at Hato Masaguaral, Guarico, Ven

ezuela, in 1993, were used for comparisons.

For radiography and blood sampling, the

tamand?as were anesthetized with ketamine

(Ketaset, Ayerst, St. Laurent, Quebec H4R

1J6, Canada), 11 mg/kg, and xylazine

(Rompun, Bayvet, Etobicoke, Ontario

M9W 1G6, Canada), 0.8 mg/kg i.m. Blood was collected from the ventral coccygeal vessels into lithium-heparinized tubes. Plas

ma calcium and phosphorus were measured

using an Ektachem analyzer (Kodak Cana

da, Scarborough, Ontario M6M 1V3, Can

ada). Plasma was frozen in liquid nitrogen

prior to vitamin analysis. Plasma vitamin A

was measured by high-performance liquid

chromatography (HPLC).1 Vitamin D me

tabolites in plasma were measured by a

competitive protein-binding assay with rat

vitamin D-binding protein (25-OHD)21 or

HPLC (l-25(OH)2D).6 Bone fluoride con

centration was measured by neutron acti

vation analysis in the University of Toronto

Slowpoke-2 nuclear reactor. Results are

given as mean ? standard deviation, and

values were compared using Student's ?-test

modified for unequal sample numbers.20

Dietary history

Initially, the tamand?as were fed a mix

ture similar to that previously recommend

ed,9 consisting of evaporated milk, com

mercial dog food, powdered protein supple ment, multivitamins, and a small number of

mealworms and crickets. In 1983, the milk

and the protein supplement were eliminat

ed, and a small amount of orange was in

cluded. The dog food was gradually re

placed by the zoo's own horsemeat-based

carnivore ration, and the level of vitamin

supplementation was gradually reduced.

Between 1984 and 1986, commercial mon

key chow (Purina High-Protein, Ralston

Purina Canada, Woodstock, Ontario N4S

7K5, Canada) was included in the diet. Be

tween 1987, when the problem was first

identified, and 1994, each tamandu? was

fed the zoo's carnivore mixture (approxi

Table 1. Dietary vitamin levels (dry matter basis) fed to captive tamand?as over a 10-yr period.

Vitamin A Vitamin D Date (IU/kg) (IU/kg)

Jul 1984 48,730 5,760

Feb 1985 58,000 6,760

Dec 1985 46,700 5,300

Feb 1986 58,000 6,270

May 1986 26,000 3,320

Jan 1987 26,300 3,190 Mar 1987-1993 22,700 1,930

mately 300 g), Vi hard-boiled egg, Vi orange, and an additional 13 IU vitamin E daily.

Dietary calcium and phosphorus levels were approximately 1% and 0.7% dry mat

ter (DM), respectively. Between 1981 and

1986, vitamin supplementation was pro

gressively reduced. Calculated daily vita

min A intake, based on reported and ana

lyzed values of ingredients, decreased from a high of 7,600 IU per animal (58,000 IU/

kg DM) to 3,650 IU (26,000 IU/kg DM). Vitamin D intake was reduced from 1,050 IU (6,000 IU/kg DM) to 440 IU (3,100 IU/ kg DM). After 1987, the diet contained ap

proximately 22,000 IU/kg DM of vitamin A and 1,900 IU/kg DM of vitamin D, rep

resenting a daily intake of 2,080 IU vitamin A and 180 IU vitamin D. Changes in di

etary vitamin A and D levels over a 10-yr

period are shown in Table 1.


Radiographie findings

Animals 1 and 3 showed severe hyper ostosis when first examined radiographical ly. There was massive hyperostosis ventral to the lumbar and thoracic vertebrae, up to

10 mm in depth, equivalent to the depth of

the vertebral body itself. Fusion of osteo

phytes had, in effect, consolidated the spine into one bone (Figs. 1, 2). Hyperostosis was

almost entirely limited to the ventral and

lateral aspects of the vertebral bodies, with

minimal ossification dorsally along the neu

ral canal, vertebral facets, or the spinous

processes. Disc space, although radiograph

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Figure 1. Radiograph of a severe case of vertebral hyperostosis in a tamandu? (T. mexicana) (animal 3),

showing massive deposition of bone along the ventral surface of the lumbar spine and the resulting kyphosis.

ically obscured by overlying bone, ap

peared to be well maintained in most lo

cations. Individual thoracic vertebrae ap

peared triangular because of r?sorption of

the cranial and caudal margins.

Hyperostosis also occurred in the cranial

portion of the tail; the individual vertebrae

became united (Fig. 3). Changes were less

marked in the distal half of the tail. The

cervical spine appeared remarkably unaf

fected despite the severity of the changes in

the thoracolumbar and coccygeal regions

(Fig. 2). No extravertebral bony changes were seen, but in one of the animals (no.

1), mineralization of the tracheobronchial

tree was apparent.

Animal 2 had a less advanced radiograph ie stage of the disease when first examined.

Osteophytes at the cranial and caudal mar

gins of the thoracolumbar vertebral bodies

had developed into pointed excrescences be

neath the vertebral discs. Bridging of these

exostoses gave the ventral surface of the

spine an undulating appearance (Fig. 4). Over the next 2 yr, the hyperostosis became

temporarily denser and more aggressive ra

diographically, with loss of integrity of the

ventral portion of the bodies of the verte

brae. Four years later, fusion was complete

but the lesion had a more benign appear ance, similar to that in animals 1 and 3.

Following the identification of vertebral le

sions in the three original tamand?as, the two

new animals (nos. 4 and 5) were monitored

radiographically for skeletal changes. Initial

ly, these animals showed no abnormalities, but radiographs taken 18 mo later demon

strated early vertebral lesions. The earliest ev

idence was a small linear radiodensity, 1 mm

in height, in the soft tissue approximately 2

mm ventral to the lumbosacral joint. Over the

next 4 yr, progressive development of radio

graphic lesions was similar in both animals.

Fifteen months later, the initial density had

enlarged to 3 mm in height and abutted the

adjacent vertebrae. Similar discrete linear or

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Figure 2. Dorsoventral view of the cranial half of the spine of a tamandu? (T. mexicana) (animal 3), showing extensive hyperostosis of the thoracic vertebrae but an absence of bony changes in the neck.

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Figure 3. Radiograph of the cranial half of the tail of a tamandu? (T. mexicana) (animal 1), showing extensive

ventral hyperostosis and adjacent soft tissue mineralization.

triangular radiodensities were visible ventral to most of the thoracic and lumbar interver

tebral joints (Fig. 5). Roughening, with small

osteophytes, was evident at the ventral mar

gins of several vertebral bodies. Linear soft

tissue calcification also developed lateral to

the coccygeal vertebrae. A progressive in crease in the size and density of the subver tebral foci, moderate lysis and remodelling of

the vertebral margins, and growth of the os

teophytes on the vertebral bodies were seen

over the next 2 yr. However, in these two

animals, no bridging of vertebral joints oc

curred as long as 5 yr after the initial exam


Examination of radiographs and reports from other institutions have documented similar lesions in other tamand?as (J. Flan

agan, Houston Zoo; J. Ott-Joslin, Woodland

Park Zoo, pers. comm.).

Clinical findings Clinical signs were evident only in the

presence of severe vertebral hyperostosis.

The most severely affected animal (no. 1) showed rear limb paresis and urinary reten

tion, which progressed to complete flaccid

paralysis within 2 wk of the initial presen tation. Animal 2 showed no evidence of neu

rologic deficit, although death may have re

sulted from a fall due to reduced ability to

climb. The third severely affected animal

(no. 3) continues to move slowly and stiffly but is otherwise mobile and able to climb.

All three of these tamand?as had kyphosis, which is typical of the normal posture of the

species but could not be straightened under

anesthesia. No signs have been seen to date

in the other two animals, despite moderate

radiologie evidence of hyperostosis.

Clinical pathology

Plasma calcium level (x ? SD) in 31

samples taken from five captive animals over 5 yr, concurrent with the development of bony lesions, was 2.6 ? 0.4 mmol/L

(range, 1.7-3.6 mmol/L) (Table 2). Four

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Figure 4. Lateral radiograph of the thoracic spine of an affected tamandu? (T. mexicana) (animal 2) at an

intermediate stage in the development of hyperostosis. Exostoses on the vertebral margins are enlarged and

fused, giving an undulating appearance to the ventral border of the spine.

samples taken from animals 3, 4, and 5 in

1989 were >:3.0 mmol/L, as were three

samples taken from animal 5 in 1990. Both

samples taken from animals within 1 mo of

arrival (animal 3 in 1981 and animal 4 in

1986) showed calcium levels <2 mmol/L.

Plasma phosphorus level in 28 samples from the same five animals over the same

5-yr period was 1.4 ? 0.6 mmol/L (range, 0.7-2.1 mmol/L). Calcium and phosphorus levels in nine wild tamand?as were 1.9 ?

0.4 and 1.6 ? 0.7 mmol/L, respectively (Ta ble 3), but these values did not differ sig

nificantly from the corresponding values in

the captive tamand?as (?-test). The 1,25-dihydroxyvitamin D level in 18

plasma samples from five captive taman

d?as was 49 ? 31 pmol/L. One animal (no.

2) showed higher levels (193 ? 29 pmol/L in three samples). The 25-hydroxyvitamin

D level in 18 samples from five animals was 55 ? 28 nmol/L.

Plasma vitamin A level in 14 samples from four captive tamand?as was 0.8 ?

0.18 |xmol/L. Serum vitamin A in two other

animals from the Woodland Park Zoo

showed even higher levels (2.2 and 3.3

|xmol/L). The mean liver vitamin A level in two samples taken from the one tamandu?

tested was 1,299 jxg/g. An affected female

tamandu? from Woodland Park Zoo had a

liver vitamin A level of 3,981 u,g/g. The

postmortem bone fluoride level in one ani

mal was 6.0 mM fluorine/M calcium.

Pathology findings

Animal 1 was euthanized due to posterior

paralysis, consistent with a direct effect of

the vertebral changes impinging on the spi nal cord. Necropsy findings included atro

phy of the limb musculature and a greatly distended bladder. The vertebral column

from the thoracic inlet to the tail had very little flexibility. Most vertebrae had multi

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Figure 5. An early stage in the development of vertebral hyperostosis in a tamandu? (T. tetradactyla) (animal

4), showing development of linear and triangular densities (arrows) ventral to the lumbar inter vertebral joints.

pie exostoses and were incorporated into a

solid bony mass (Fig. 6). Ankylosis was

primarily ventral to the vertebral bodies, al

though some fusion of exostoses had oc

curred more dorsally around the vertebral

facets. The most dramatic changes were

present in the thoracic vertebrae. Extensive

localized lysis of one vertebra had led to

complete degeneration of the vertebral body and collapse of the adjacent intervertebral


Histologically, the vertebral lesions con

sisted of irregular areas of cartilage, fibro

cartilage, dense collagenous fibrous tissue, and occasionally woven bone. In some sec

tions, adjacent to these exostoses there were

masses of eosinophilic necrotic debris.

Small foci of soft tissue calcification were

evident on the myocardium and on the sur

face of the spleen. Focal mineralization was

also present in the tunica media of the aorta

and some smaller vessels. Occasional renal

medullary tubules were mineralized.

In animal 2, death was a result of hem

orrhagic shock from a ruptured liver, which was likely a sequel to congestive heart fail ure. There was extensive exostosis and an

kylosis of the vertebral bodies from the tho

racic inlet to the tail, with fusion of the ver

tebral column between these points.

Histologically, there was hepatic conges tion and hemorrhage, and myocardial de

generation with focal mineralization. Mem

branoproliferative glomerulopathy was

present with scattered glomerular mineral

ization and occasional mineralized tubular

casts. Mineralization of the bronchiolar car

tilage was also noted. The normal ventral

borders of the vertebrae were obscured by

compact acellular swirling osteoid with nu

merous metabolic arrest lines and large amounts of hemopoietic marrow. Within

this matrix were small islands of degenerate

hypereosinophilic cartilage and osteoid.

The dorsal and lateral aspects of the verte

brae were minimally affected.

Page 9: Vertebral Hiperostrosis


Table 2. Plasma calcium, phosphorus, 1,25-dihydroxy vitamin D, 25-hydroxyvitamin D, and vitamin A levels

in five captive tamand?as.

Ca P l,25(OH)2D3 25,(OH)2D3 Vit A Animal no. Date (mmol/L) (mmol/L) (pmol/L) (nmol/L) (|xmol/L)

1 Mar 87 3.4 1.3 8 58 2 Aug 88 2.1 1.6 172 38 Dec 88 1.9 1.4 204 37 1.2 Oct 89 2.4 4.1

3 Oct 81 2.1 2.2 43 36

Jan 82 2.1 2.0 79 136

Mar 87 2.2 1.8 16 23 Nov 89 3.0 1.1 0.9 Dec 89 3.2 1.4

Sep 90 2.3 60 46 0.6 Oct 90 2.3 1.4 39 65 1.1 Feb 92 2.4 1.7

4 Dec 86 1.8 2.1 50 4

Jan 87 2.5 1.4 12

Aug 88 2.3 1.0 26 32 1.0 Nov 89 3.5 1.3 0.7

Sep 90 2.4 53 66 0.8 Oct 90 2.2 1.6 100 66 0.7

Mar 92 2.4 1.6

5 Jan 87 2.2 1.2 86 80

Aug 88 2.4 1.1 18 49 0.6 Nov 89 3.6 0.8 0.7

May 90 3.0 0.9 102 61 0.7

May 90 3.0 0.8

Jun 90 2.6 0.7 0.8 Jul90 2.6 1.1 26 71

Aug 90 3.0 0.8

Sep 90 2.3 70 0.8 Oct 90 2.7 1.4 60 67 0.8

Nov 90 2.8 1.0

Mar 92 2.5 1.4

x 2.6 1.4 49 55 0.8

SD 0.4 0.6 31 28 0.18

n 31 28 18 18 14


The nature, history, and distribution of

the bony lesions in the tamand?as at MTZ

and the occurrence of cases in other insti

tutions point to a common etiology. The ra

diologie and pathologic findings strongly

suggest a nutritional cause related to calci um metabolism. Hyperostosis of the axial

skeleton is the predominant characteristic.

Soft tissue calcification in the necropsied animals was extensive and considered part of the syndrome.

Despite extensive vertebral hyperostosis,

kyphosis, and reduction in mobility, neu

rologic signs were limited. Rear limb pa resis was seen in only one animal in an ad

vanced stage of the disease, indicating that

spinal cord and segmental nerve function are not compromised until hyperostosis be comes extensive. Focal dorsoventral flatten

ing of the spinal cord was seen, but only one small bony spicule in the dorsolateral

part of the canal was evident. New bone

formation was predominantly ventral, as

seen in the prepared specimen (Fig. 6). The

location of the early radiographie lesion

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Table 3. Plasma calcium and phosphorus levels in

nine wild tamand?as (T. tetradactyl?).

Ca P Animal no. (mmol/L) (mmol/L)

6 1.6 1.2

7 1.4 1.6

8 1.3 1.0

13 1.9 3.0

15 2.2 2.3

16 2.2 1.3

17 2.5 1.6

18 2.2 0.9

20 2.2 1.7

x 1.9 1.6

SD 0.4 0.7

suggests that calcification first develops in

the ventral longitudinal spinal ligament. The myocardial degeneration, glomerulo

pathy, and soft tissue mineralization prob

ably relate to the age of the animals and to

chronic hypercalcemia. The pathologic changes were suggestive

of hypervitaminosis A or D. Excessive vi

tamin A intake has been incriminated in cases of deforming spondylosis of the cer

vical vertebrae in domestic cats.19 There are,

however, some differences between the

changes seen in cats and those in the ta

mand?as. In feline hypervitaminosis A, ex

ostoses develop principally on the dorsal

and lateral aspects of the cervical vertebrae,

rarely ventrally, and proliferations will

readily impinge on the intervertebral foram

ina to affect the segmental nerves. The tho

racic vertebrae, ribs, and axial skeleton may also be affected. In contrast, the ventral as

pect of the thoracolumbar spine is the pri

mary site in the tamand?as. Periosteal cal

cification and skeletal hyperostosis are also seen in adult humans as a feature of vitamin

A toxicosis, although the spine is rarely in

volved.4-17 The histopathology was similar

to that in cats with hypervitaminosis A.

Plasma vitamin A levels in the taman

d?as were at the lower end of the ranges

Figure 6. Prepared specimen of the lumbar spine of an affected tamandu? (T. mexicana) (animal 2), showing ventral and lateral hyperostosis and fusion. Note that the apophyseal joints are unaffected.

Page 11: Vertebral Hiperostrosis


considered normal in other species (rat =

1.5 |xmol/L; human = 0.7-1.0 |xmol/L; cat = 0.7-2.8 |xmol/L) and did not approach the levels usually considered toxic (>3.5

Ixmol/L).11-12'19 However, there may be little

correlation between plasma vitamin A lev

els and liver stores.12 The liver vitamin A

stores were higher than the normal levels

usually seen in other species, although they were still well below the values associated

with hypervitaminosis A in cats (8,500

40,000 |xg/g).81119 Standard mammalian liv

er vitamin A concentrations are 50-300 |xg/

g, but polar bear livers may contain as

much as 30,000 |xg/g.812 The upper safe limit for dietary admin

istration of vitamin A in other species is

about 10 times the normal daily require ment, i.e., 20,000 and 100,000 IU/kg diet.12

The initial dietary vitamin A levels were

potentially toxic for some domestic species. After 1987, the dietary level of approxi

mately 22,000 IU/kg is consistent with that

provided to many carnivorous species, al

though still several times the daily require ment for most mammalian species.8

In humans, hypercalcemia occurs in a

minority of cases of vitamin A intoxica

tion.3417 In feline hypervitaminosis A, hy

percalcemia does not appear to be present, and the levels of calcium and phosphorus in the diet have little influence on the de

velopment of exostoses in the cat.2-5 A few

of the individual plasma calcium values

from the affected tamand?as would be con

sidered hypercalcemia in other species, but

the overall mean is comparable with that of

other mammals, including the limited num

ber of reports for captive anteaters.7 22


reported values were obtained from captive animals fed similar diets. Samples taken

from nine wild T. tetradactyla in 1993 had

a mean plasma calcium value of only 1.95

mmol/L (Table 3), but this value was not

significantly different (i-test) from that of

the captive animals. The levels found in an

imals soon after arrival were lower than

those measured later. The levels found in

the long-term captive animals could repre

sent hypercalcemia in this species, which

would be supported by the presence and

distribution of the soft tissue mineraliza

tion. The tamandua's diet of invertebrates

suggests a low calcium intake.1415 Further

studies are in progress to evaluate normal

calcium levels in this species. Levels of vitamin D metabolites were

within the normal ranges for humans and do

mestic animals, except for animal 2, which

showed elevated levels of l,25(OH)2D and

normal serum calcium and is the only result

suggesting hypervitaminosis D. One sample taken from one animal (no. 4) shortly after

arrival was considered to be deficient in vi

tamin D, but interpretation of these blood val

ues is hampered by a lack of knowledge of

normal values for these animals. Normal lev

els of 25-hydroxyvitamin D in other mam

mals are between 25 and 80 nmol/L (10-30

ng/ml), increasing to 500-1000 nmol/L in

toxic states. Normal 1,25-dihydroxyvitamin D levels are between 25 and 100 pmol/L

(10-45 pg/ml).8'12

Very little information exists on the max

imum safe dietary level for chronic expo sure to vitamin D in any species, although it is generally accepted that disorders of

metabolism and increases in serum vitamin

D metabolites will occur at intakes of 20

times the daily requirement, which in most

animal species is in the range of 200-1,200

IU/kg diet.12 Based on studies in other spe

cies, chronically ingested levels below

2,200 IU/kg DM should be safe, but there

is considerable species variability. The vi

tamin D levels initially fed to the taman

d?as (6,000 IU/kg) would have been poten

tially toxic for other species, and even the

reduced level fed since 1987 (2,000 IU/kg) is 2-10 times the requirement for other

mammals and is at the high end of the safe


Most of the effects of hypervitaminosis D are due to chronic hypercalcemia, result

ing in metastatic calcification, particularly in the major arteries, gastric vessels, and

renal tubules. Mineralization of the bron

chial cartilage, alveoli, and bronchial sub

Page 12: Vertebral Hiperostrosis


mucosa may also be seen.13 Although cor

tical thickening and bone sclerosis also oc

cur in vitamin D toxicosis, typically with

the production of abundant basophilic ma

trix and obliteration of the medullary cav

ities of the long bones, proliferative bone

disease as seen in the tamand?as is not a

feature of vitamin D intoxication in other

species, including humans.1317 In the taman

d?as at MTZ, soft tissue mineralization was

present in both necropsy specimens at many of these typical locations. Postmortem re

cords from other institutions indicate that

soft tissue calcification occurred quite fre

quently, but vertebral hyperostosis was seen

(P. Wolff, J. Letcher, J. Flanagan, and J. Ott

Joslin, pers. comm.). Variations in vitamin

A and vitamin D supplementation between

institutions probably account for the differ

ences in presentation.

The condition in these anteaters is similar

to diffuse idiopathic skeletal hyperostosis (DISH) in humans. DISH is a discrete skel

etal disorder of middle-aged and older peo

ple manifested by a number of clinical and

radiographie criteria, including the presence of flowing calcification and ossification

along the anteroventral (in human termi

nology) aspect of at least four contiguous vertebral bodies, particularly in the thoracic

spine, in the absence of other evidence of

inflammatory disease or degenerative disc

disease.18 A similar condition has been re

ported in a dog.10 In many cases, extraspinal

calcification and exostoses are also seen.

The predominant, and likely initial, lesion

in DISH is calcification or ossification of

the anterior (ventral in animals) longitudi nal ligament of the spine, in some cases in

the absence of vertebral lesions, hence the

earlier terminology spondylitis deformans

ligamentosa. This is also the location of the

earliest visible lesion in the tamand?as. The causes of DISH are unknown, although ge netic factors may be involved.

Chronic fluorine intoxication or fluorosis

may also be characterized by vertebral os

teophytosis as part of a syndrome of mul

tifocal periosteal proliferation.16 Vertebral

hyperostosis in fluorosis develops at several

locations on the vertebrae, including the

spinous processes and the posterior (dorsal) intervertebral ligament, and is more likely to cause neurologic impairment. Periosteal

proliferation will also be seen in the appen dicular skeleton. The bone fluoride level in

the one tamandu? tested was within the nor

mal range for humans and domestic animals

(K. Pritzker, Univ. Toronto, pers. comm.).

The slow progression and limited radio

graphic changes in the newer animals over a 5-yr period contrasts strongly with the

massive hyperostosis and soft tissue calci

fication that occurred in the original ani

mals over a similar period, suggesting that

the reduced amount of vitamin supplemen tation since 1987 is safer than that offered

previously but still produces toxic levels.

The original animals were a different spe cies from the newer animals, but the differ ences between the two species are limited to minor anatomical variation and are not

considered significant factors.

A survey of diets fed to giant anteaters

(Myrmecophaga tridactyla) in zoos re

vealed a wide variation in calculated nutri

ent values (R. Patton, pers. comm.). Vita

min A levels were 1,900-60,000 IU/kg, vi

tamin D levels were 308-7,260 IU/kg, cal

cium was 0.7-2.0% DM, and phosphorus was 0.37-1.1% DM.

The bony and soft tissue lesions in the

tamand?as probably were due to excessive

intake of vitamin A, perhaps compounded

by a higher than necessary intake of vitamin

D. We recommend that levels of vitamin A

and vitamin D in anteater diets be restricted to less than 8,000 IU/kg DM and 800 IU/

kg, respectively, and the level of calcium

should be restricted to 1.0% or less. Studies are currently being undertaken on the nutri ent intake of these species in the wild.

Acknowledgments: We thank Drs. Sandie

Black and Virginia Honeyman for the pathologic examinations; Drs. Ken Pritzker and Reinhold

Vieth for fluorine and vitamin D analyses, re

spectively, and for their advice; Dr. Carlos

Bosque, Maribel Hernandez, and the staff of the

Page 13: Vertebral Hiperostrosis


Fundaci?n Nacional de Parques Zool?gicos y

Aquarios in Venezuela for their cooperation in

the collection of the blood samples from wild

animals; and Mr. Tomas Blohm for providing

facilities at Hato Masaguaral. Drs. Janis Ott-Jos

lin, James Letcher, and Joe Flanagan provided

data from the Woodland Park, Lincoln Park, and

Houston zoos, respectively.


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Received for publication 1 March 1994