Veterinary Quarterly

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Delayed swayback in goat kids, a study of 23 cases

W. Wouda, G. H. A. Borst & E. Gruys

To cite this article: W. Wouda, G. H. A. Borst & E. Gruys (1986) Delayed swayback in goat kids, a
study of 23 cases, Veterinary Quarterly, 8:1, 45-56, DOI: 10.1080/01652176.1986.9694017
To link to this article: https://doi.org/10.1080/01652176.1986.9694017

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 Delayed swayback in goat kids, a study of 23
cases
W. Wouda', G. H. A. Borst2, and E. Gruys'

SUMMARY The results of a retrospective study of 23 goat kids with delayed swayback are reported.
Principal clinical signs were ataxia, loss of postural control, spasticity of the hindlimbs, and muscular
weakness, often progressing to permanent recumbency. Denervation of skeletal muscles was demon-
strated by electromyography in 2 kids. Three kids slowly recovered during hospitalisation.
Histopathological changes were characterized by degeneration of selected neuronal populations with
their processes within the central and the peripheral nervous system. Affected systems included upper
motor neuron, vestibular, general proprioceptive, and lower motor neuron pathways, with additional
involvement of the cerebellar cortex in some animals. Our findings, including limited ultrastructural
observations, support the notion that the neuraxon rather than the myelin sheath is the prime target of
disease in delayed swayback. The available copper values of affected kids and their unaffected herd
mates were significantly lower than those of random control goats, which provides furt her support for a
role of copper deficiency in the aetiology of this disease in the goat.

INTRODUCTION with those of sheep, but it is now known

Swayback or enzootic ataxia is a well
known neurological disorder in lambs. A
congenital and a delayed form of the dis-
ease can be distinguished. In the latter form
clinical signs appear from about one week
to six months after birth (3). Copper de-
ficiency has been shown to play a major
aetiological role in this disease (25).
Since 1962 several case reports from
Europe (4, 5, 16, 18), North America (8, 22,
23), Australia (14, 15, 19) and Africa (13)
have attracted attention to a similar disease
entity in goat kids. As in lambs, the disease
in goat kids is characterized by a typical
histological picture of neuronal alteration
and myelin degeneration in the brain stem
and spinal cord. Unlike in lambs, cerebel-
lar hypoplasia has been a frequent addi-
tional finding in goat kids (5, 8, 14, 15, 16, 19,
22). In goats the disease has also been asso-
ciated with hypocuprosis (4, 13, 15, 19, 23).
However, some authors are inconclusive
about the role of copper deficiency in the
aetiology since ranges of copper values in
both clinically normal and affected kids are
wide and often overlap (5, 8, 16, 22). Goat
copper values have usually been compared
that there are fundamental differences in
copper metabolism between goats and
sheep (21).
In this report we present the results of a
retrospective study of 23 goat kids with
swayback-like signs and/or lesions. A com-
parison of copper values of affected kids
and their herd mates with those of random
control goats, strongly suggests that a low
copper status is involved in the aetiology of
the disease.
MATERIAL AND METHODS
All 23 kids were submitted for clinical and/or patho-
logical examination during the period 1973-1983. The
kids originated from 13 properties, scattered all over
the Netherlands. All kids were normal at birth and
during early postnatal life. The age at onset of signs
varied from 5 to 28 weeks, with a mean of 13 weeks
(Table I). Progressive motor disturbances were seen
in all kids. A staggering gait, abnormal straddle-leg-
ged posture, imbalance, and sometimes rigidity of the
hind limbs were the first signs noted by the owners.
Weakness with frequent collapse usually followed,
until the animals became permanently recumbent and
rapidly developed flexor contracture of the forelegs.
In 3 kids the forelimbs were affected prior to the
hindlimbs.

Department of Veterinary Pathology, State University of Utrecht, Yalelaan 1, 3508 TD Utrecht, the
Netherlands.
2 Regional Animal Health Service Centre Overijssel, Zwolle, the Netherlands.

THE VETERINARY QUARTERLY, VOL. 8, No. I, JANUARY 1986 45

."
 Most kids remained alert and ate well. Seven kids
were euthanized with an overdose of barbiturate
shortly after presentation. The others were hospital-
ized for periods varying from 2 days to 9 weeks, after
which they were either discharged or euthanized. Two
kids died spontaneously during hospitalization.
Clinical, neurological, haematological and faecal
examinations were carried out in most cases. Needle
electromyography was done in kids 21 and 22.
Twenty kids were necropsied. Tissues were fixed in
10% buffered formalin. Brains and spinal cords were
sliced transversely after fixation and blocks were
sampled at various levels. Serial blocks were taken
from the brain stem in kids 17, 21, 22, and 23. After
embedding in paraffin, 6 pm sections were cut. The
following staining methods were used: haematoxylin
and eosin, luxol fast blue-cresyl echt violet, Holmes
silver, Holmes silver and luxol fast blue, Nissl, Holzer,
and Weigert-Van Gieson. In goat 17 small portions
from the cervical intumescence of the spinal cord were
removed immediately after death and fixed in 4%
glutaraldehyde. Specimens were postfixed in 2%
osmiumtetroxide and embedded in araldite. Semi-
thin sections were stained with toluidin blue. Ultra-
thin sections from selected areas were contrasted with
uranyl acetate and lead citrate and examined with a
Philips 201 electron microscope.
Blood copper values were determined in 5 affected
kids, 5 dams, 11 adult herd mates and 4 of their
unaffected kids, at 3 properties. Liver copper values
of 7 affected kids were determined postmortally. In 2
affected kids a liver biopsy was taken for copper
analysis. In order to get reference values, copper ana-
lyses were done on 35 blood samples and 57 liver
samples from immature and adult goats without a
history of locomotor disturbance. Blood samples
were collected from experimental goats at the Univer-
sity and from slaughter goats. Liver samples were
collected from goats randomly submitted for autopsy
and from slaughter goats. Copper analyses were car-
ried out by atomic absorption spectophotometry,
using an air-acetylene flame, after destruction of the
organic material by concentrated nitric and sulphuric
acids. The Mann-Whitney 13 test was used for statis-
tical comparison of the copper values of both young
and adult goats from properties with swayback, with
those of the control goats.
RESULTS
Clinical examination and treatment
Principal clinical data for each kid are
summarized in Table 1. Most kids were
recumbent at the time of submission and
were hardly or not able to support body
weight. Many of them showed secondary
flexor contracture of the forelimbs. Some
recumbent animals showed periodic spas-
modic contractions of the hindlimbs (Fig.
1). Goats which were ambulatory at the
time of presentation showed ataxia and pa-
resis, sometimes with spasticity in the hind-
limbs and overstretched tarsal joints. Hy-
46
permetria, imbalance, head tremor, and
laryngeal stridor were other signs noted in
individual kids.
Electromyography in kids 21 and 22
showed fibrillation potentials and positive
waves in various proximal limb muscles.
Diarrhoea was seen in some animals. In
more than half of the cases large numbers
of oocysts were found in the faeces and
occasionally also Strongylus type eggs. In 6
kids a slight anaemia was found on haema-
tological examination.
Hospitalized kids received nursing care
and physiotherapy, including exercise, and
passive movement and massage of affected
legs. Coccidiostatic treatment was given if
necessary. Kids 3, 7 and 15 showed im-
provement during hospitalisation and were
send home after 3-6 weeks, where they re-
covered reasonably well. Kids 21 and 22
received intramuscular applications of
copper, after which no further progress of
the disease was seen. In all other kids clini-
cal signs either remained stationary or de-
teriorated. The remaining goats at prop-
erty J received parenteral copper supple-
mentation, after which no new cases occur-
red. On properties E and M no further
cases were seen after replacement of the
sheep concentrate with a concentrate for
cattle and horses respectively.
Pathomorphological findings
At necropsy most animals were emaciated
and showed various degrees of muscular
atrophy, sometimes with scattered pale
fibre groups. In some kids coccidiosis and
gastrointestinal helminth infestation were
found. No macroscopic lesions were seen
in the central nervous system.
In all cases similar microscopic lesions
were present in the brain stem and spinal
cord, with differences only in intensity and
chronicity between individual kids. The
lesions consisted of degeneration of both
nerve cells and fibres in a characteristic
bilaterally symmetrical pattern.
Altered neurons were found in the nucleus
ruber, vestibular nuclei (especially the lat-
eral), reticular formation of the medulla,
ventral horns of the spinal cord (especially
the lateral motor nuclei at the level of the
cervical and lumbosacral intumescences),
and the thoracic nuclei (Clarke's columns).
THE VETERINARY QUARTERLY, VOL. 8, No. 1, JANUARY 1986
....
; Table I. Signalment and clinical history of 23 goat kids with swayback.
iii
< Kid Property Breed Sex Litter Age at Duration Clinical presentation
m
m number size onset (weeks)
(weeks)
>
m 1 A Afr.dwarf U U + 8 + 4 Recumbent, unable to stand
,
XD
c 2 B Afr.dwarf 2 5 6 Recumbent, spastic movement of hindlegs, flexor contracture of
Z ]
forelegs
m 3 B Afr.dwzir 2 11 3 Ambulatory, slight hypermetria, imbalance after blindfolding,
m
slow recovery
4 B Afr.dwarf 2 6 7 Recumbent, extensor spasm of hindlegs, body tremor, flexor
< contracture of forelegs
2 U 12 9 Recumbent, unable to stand
5 C* Dutch white
oo

Z 6 D Afr.dwarf 2 7 2 Recumbent, able to stand with assistance, paresis of hindlegs,

P ]
flexor contracture of forelegs
1 7 D Afr.dwarf 2 7 4 Ambulatory, tetraparesis, slow recovery
> Ambulatory, ataxia and paresis of all 4 legs
8 E Afr.dwarf 2** 8 4
4
5.'

Tc 9 E Afr.dwarf 2 8 4 Ambulatory, ataxia and paresis of hindlegs

]
..o
ou 10 E Afr.dwarf 2 8 4 Ambulatory, ataxia and paresis of hindlegs
ce

11 1' Afr.dwarf 2 17 4 Recumbent, able to stand with assistance, imbalance, flexor

contracture of forelegs
12 G Afr.dwarf 3 20 4 Recumbent, hypotonia of hindlegs, flexor contracture of forelegs

13 G Afr.dwarf 2 21 4 Recumbent, hypotonia of hindlegs, flexor contracture of forelegs

1

14 G Afr.dwarf 2 21 4 Recumbent, hypotonia of hindlegs, flexor contracture of forelegs

15 G Afr.dwarf 2 20 12 Recumbent, flexor contracture of forelegs, slow recovery

16 1 28 2 Recumbent, Able to stand with assistance, spasticity of hind-

H Afr.dwarf
17 H Afr.dwarf
18 I Dutch white
legs, spinal reflexes and pain sensation decreased
3 12 4 Ambulatory, paresis primarily of forelegs, spinal reflexes
decreased
3 11 2 Recumbent, unable to stand, hypotonia, urinary incontinence

19 J* Dairy cross 1 8 8 Recumbent, hypotonia primarily of forelegs

20 K Afr.dwarf 1 8 1 Ambulatory, tetraparesis, laryngeal stridor

21 L Dutch white 2 17 10 Recumbent, paresis primarily of forelegs, flexor contracture of

) forelegs
22 L Dutch white 2 17 10 Ambulatory, ataxia and hypermetria of hindlegs, decreased spinal
reflexes and pain sensation of hindlegs
23 M Afr.dwarf 1 8 16 Ambulatory, ataxia and paresis of hindlegs, head tremor

4=.
U: unknown, *: more kids at property affected, **: twin kid also affected, I: litter mates
 inTrr-4.
.
. j
o:tY.
-,
_ - 41
I, r if
p.
I
- legs. Spastic extension of the
$ ".
..4.9(-4 -;
1.:%\ °
. .
ar.44:1Jrt.
°
r :
The predominant neuronal change was cy-
toplasmic swelling and chromatolysis,
ranging from central chromatolysis with
eccentric location of the nucleus to com-
plete disappearance of Nissl substance
with disruption and loss of nuclei (ghost
cells). Other neurons showed shrinkage
and eosinophilic fibrillary transformation
of the cytoplasm, often with nuclear pyk-
nosis or fading (Figs 2, 3). In the latter
neurons an increase of neurofibrils could
be demonstrated by silver impregnation
(Fig. 2b), while ghost cells showed lysis of
neurofibrils. Neuronophagia was sporadi-
cally seen (Fig. 3b). Axonal swellings were
frequently observed, especially in the proxi-
mity of altered neurons in the ventral
horns of the spinal cord (Fig. 3c). These
swellings contained excess neurofibrils. In
chronic cases neuronal loss with associated
glial proliferation was'apparent.
White matter changes were most conspicu-
ous in the spinal cord, especially in the
dorsal part of the lateral funiculus and in
the ventral funiculus adjacent to the ven-
tral median fissure, with less severe chan-
ges between these areas (Fig. 4a). Lesions
consisted of degeneration and loss of my-,
elinated axons, with associated phagocytic
and glial reactions (Fig. 4c). In kid 23 the
whole ventrolateral funiculi showed severe
fibre loss, particularly in the thoracic re-
gion. Rarely were affected fibres seen in the
dorsal funiculi. Similar changes were seen
in the lower brain stem. A tentative neuro-
anatomic analysis revealed the involvement
of the dorsal spinocerebellar tracts, which
were traceable up to the caudal cerebellar
peduncles, the ventral spinocerebellar
48
.Tor c -7-,-
7.1:
j
c.
I
Fig. I. Lateral recumbency.
Flexor contracture of the fore-
N
hindlegs (kid 4).
m'f431.: ,,.
tracts, the rubrospinal tracts, the vesti-
bulospinal tracts, and the medial longitu-
dinal fascicles (Fig. 7).
In kids 2, 5, 8, 11, 13, 20, and 23 additional
lesions were present in the cerebellum.
These lesions ranged from patchy or diffuse
degeneration and loss of Purkinje cells to
folial atrophy affecting all cortical layers.
Both the vermis and hemispheres were in-
volved. Altered Purkinje cells showed chro-
matolysis, vacuolisation and hyalinisation.
Fusiform swellings of the proximal axon
(torpedoes) were occasionally observed. In
areas of Purkinje cell loss a reactive prolifer-
ation of the Bergmann glia was evident
(Fig. 5a). In atrophic folia there was loss
and dystopia of Purkinje cells, cellular
paucity of the internal granular layer, and
narrowing of the moleCular layer (Fig. 5b).
An increased cellular density, partly due to
microglial activation, was seen in the folial
and central white matter of affected cere-
bella.
Other changes noted in the central nervous
system were polymicrocavitation of the ex-
ternal thalamic laminae in 4 cases, and
gliosis of the ventral thalamic nuclei and
superior olivary nuclei respectively, in 2
cases.
In all kids Wallerian type degeneration of
varying intensity was seen id the ventral
spinal nerve roots (Fig. 6a), especially at
the level of the cervical and lumbosacral
intumescences. Similar lesions were seen in
mixed peripheral nerves of the limbs (Fig.
6b), and the spinal root of the assessory
nerve. In kid 20 Wallerian degeneration
was seen in the recurrent laryngeal nerve.
THE VETERINARY QUARTERLY, VOL. 8, No. I, JANUARY 1986
 44.11K",e
II
4,4
7.'7
:
e
s
. "4".% 4e ;vri!
\ I.
.. ."- . . ' 0
'1
4
- 6'1. .
10,1, ;, T.
rlL 'fe
-.
A

14? ;?. '4)

;
r4.
A4 2 A -
...:..- - '- .

1
- 11
9 ,

...,,,
;. ,....
,,_
?A 1
.... --. ._ ...
' ,,
,

-i .: A: :,- 1,,
I . #.%, b ..
. I0
. ` --. I ' ...
r IN' 44 L ::. . \
, . 40.'
,,, `
1 , ,.. .j .
11

d
..)
9.
-
ell
.
%!

.. ,
,

..
.

.
i ,i S.6
1 `A
0
A'

tt4'
BcSIs

P
, . 1-1; ,f.
l ',.
Illlor . to . u.
. Ni
,i '. '
' to . 4,1_

411-1,,.' ,,,,, '. 4. ":. ... ,.. '

ti''''15.*" . : *
1

'I, .,c C,.4 , - -

0 Q14 A .. c:- ".... .
,,,,

,.
'_ '
t.t
,....., . S -.
:.,..---... ,...-
. I.
i-.1.,"te. il . ' A __Limo IJ
a. b.
Fig. 2. Lumbosacral intumescence of the spinal cord. Ventral horn. Neuronal alterations (kid I I). a. Central
chromatolysis (A), eosinophilia and shrinkage (B), complete chromatolysis and regression of the nucleus (C).
Haematoxylin and eosin, x 200. b. Increase of neurofibrils in neuronal cell body (D), and in axonal process (E).
Lysis of neurofibrils in ghost cell (F). Holmes silver, x 400.
_

OP' I

. ;

-;

1.1

_
;
;4`
A.
Avit%r' til ,

;Sr'"44,,A;;)
tt.;.%
141e:
4074,,,,V*^V
ri

b. C.

Fig. 3. Spinal cord grey matter. Ventral horn.

a. Central chromatolysis (kid 19). Nissl, x 400.
b. Neuronophagia (kid 17). Haematoxylin and eosin, x 600.
c. Proximal axonal swelling (kid 2). Haematoxylin and eosin, x 400.

THE VETERINARY QUARTERLY, VOL. 8, No. 1, JANUARY 1986 49

 16.7,47'..CC ..7,40:::#48,-) NI,,,
:°, tser ' .. '. r: 0,
. -., ....- t.- $!;,,k,. c ... 4
. 4:-,.......: . .... Ai.,
4 41 -,- .1.t.40.--.. .11 11,04
! .Z.V 47. v 40. 0 1, ' . V'''' .444

.4 ,.. Ls,
;
1
illi%.,...,..41::44:411.:;:gletw ..::**164.47,16.14144tia;

T
0 %.414;T:iWelt,t';g: ,.'s

, Itt...A ,tnea.t......,fi
b.
" ,-
v., "". .,e--4.,
ts ....
": e:.. d'46
%
p
t.
n
t% t, 4 %4 1 '' 4t<%1;1f

eA 4
er
4
a. c.
Fig. 4. Cervical spinal cord (kid 4).
a. Symmetric loss of myelinated fibres, especially in dorsolateral tracts (arrows), and less conspicuously in
ventromedial white matter (arrowheads). Luxol fast blue, x 10.
b. Unaffected dorsal white matter. Holmes silver, x 400.
c. Dorsolateral white matter: loss of axons. Holmes silver, x 400.

. .`
., . ',..! t4";
--- 7.,... .,...- S.

Se
5* ./A.
.

op .
4..te,,
..., , .... .
. t,
t, :11..
" . .` .
,C55t. w
1. e
.
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0 I.
.
:
4 ' ... s .. ,
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...,

i'.. :1 .. 'if,
. *.
'5,..."
1 t1 ' , . ....` 1
c..1

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,

4.:
* k:.:.......z: ...Vg .,::.
-:, . I 4'

....4.1,- ,ft''
jr
-
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r
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.--s .,..,,
15 1 4it '241. If5 1..' '`;" . o.0,- ;
..:, 7. . -1 . .,
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c,.. 1; 1
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-
1
,,
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VIP
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1.;.1
tCX611,414 c
.A
,
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- -_.,i I t 00.:sel
* .I
Ike 1
o
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m,

64* 11s
k
: -.., to:4 N ke l'i-
ir A ° ;0. , . .. ,
'."-:.**1
... '.°3
. ' ..;
..
.
4
le* '7, 0. 411 .0;0
,, 6°,6° ..t s. IN.
* t,
oe-w
; 14.4
s
di t P' t,
t`40.7 "
1
;
..,'"'('Oe 6' : !..f
0 Potty ,5,, " ..;I:;
441± ,t-P. -.41P
1.14, J1 ,. I .

- .,_s 1.70; v,o'N e

.14o. terk.1- s I 4: 4."A a 4,
-se,.`f 4114 411* 16 r °it
.p.
*
..., ,...;. ...____. ... .40
t 1114,
Mo .4,f.
11*
I ,C /44.014
01.,1"--._4161.101. 0 114 e..ot ` _
4, . i
a. b.
Fig. 5. Cerebellum. a.Purkinje cell loss with associated proliferation of Bergmann glia (kid I I ). Hacmatoxylin
and eosin, x 200.
b. Cerebellar cortical atrophy: Purkinje cell loss and dystopia, narrowing and cellular paucity of internal
granular layer (kid 2). Haematoxylin and eosin, x 200.

50 THE VETERINARY QUARTERLY, VOL 8, No. 1, JANUARY 1986

 .:, -"'

0,--
.44:As;

-NOW
..0-"`
b.
".

a. C.

Fig. 6. a. Lumbar spinal nerve roots (kid 16). Fibre degeneration and loss in ventral root, contrasting with
normal dorsal root. Luxol fast blue-Holmes silver, x 40. b. Sciatic nerve. Longitudinal section (kid 17).
Wallerian degeneration: fragmentation of myelinated nerve fibre with formation of ellipsoids, contrasting with
intact fibres. Luxol fast blue-Holmes silver, x 400. c.M. triceps (kid 21). Neurogenic atrophy: group of small
angular muscle fibres adjacent to normal sized fibres. Haematoxylin and eosin, x 400.

Skeletal muscles showed varying degrees of Electron microscopic findings

neurogenic atrophy, evidenced by the pres-
ence of groups of small angular fibres
among normal ones (Fig. 6c). No relevant
lesions were found in the other extraneural
tissues.
In a limited ultrastructural study of the
ventral grey matter of the cervical intumes-
cence in kid 17 the following changes were
noted. In neuronal perikarya dispersion of
granular endoplasmic reticulum was seen.

Fig. 7. Schematic representation of principal affected neuronal systems in goat kids with swayback. n.r. =
nucleus ruber, f.r.m. = formatio reticularis medullae, n.v.l. = nucleus vestibularis lateralis, n.m. = nucleus
motorius, n.t. = nucleus thoracicus, t.s. = tractus spinocerebellaris, t.r. = tractus rubrospinalis, t.v. = tractus
vestibulospinalis, p.m.f. = peripheral motor fibres.

THE VETERINARY QUARTERLY. VOL. 8, No. I, JANUARY 1986 51

 4;1
Ith/r2t1.1
<4-44Orf,
640'Vt. ' sss*
4441.ts,
'VI
iirs 4P,Votrerie;

%'It41
"4", 1144
w*.

toy
4 'r

a. b.

Fig. 8. Cervical intumescence of the spinal cord. Ventral horn (kid 17). Electron micrographs: a. Portion of
neuronal perikaryon. Dispersion of granular endoplasmic reticulum. Short haphazardly arranged cisterns.
Numerous free ribosomal clusters, x 11.500.
b. Large myelinated axon. Intra-axonal accumulation of neurofilaments.(Myelin sheath artificially damaged)
x 25000.

Cisterns were short, haphazardly arranged
and associated with large amounts of free
ribosomal clusters (Fig. 8a). Excess of neu-
rofilaments was seen in some neuronal cell
bodies. Dense accumulations of neurofi-
laments were observed inside large myel-
Mated axons (Fig. 8b). There was a relative
abundance of fibrous astroglial processes.
Copper analyses
Blood and/or liver copper levels of 9 affect-
ed kids are shown in Table 2. Blood copper
concentrations of the herd mates, includ-
ing 5 dams of ataxic kids, on 3 properties
are shown in Table 3. Blood and liver
copper values of the control goats are dia-
grammatically represented in Fig. 9. Blood
copper values of affected kids were signifi-
cantly lower than those of the control kids
(p < 0.001), but did not differ from the
values of kids without neurological signs
on the same property. Blood copper values
of the adult goats from properties with
swayback were significantly lower than
those of the mature control goats (p <
0.001). There was no significant difference
between the blood copper values of dams
with affected kids and the values of the
other adult goats on the same properties.
Liver copper values of affected kids were
significantly lower than those of the con-
trol kids (p < 0.001).
I
Immature control goats had significantly
lower liver copper values than the adult
control animals (p < 0.01). A consider-
able portion of them had liver copper
values in the same range as the affected
kids.

52 THE VETERINARY QUARTERLY. VOL 8, No. I, JANUARY 1986

Table 2. Blood and liver copper levels of 9 goat kids a. b.
with swayback.
0 adult goats
60
12 kid goats
Blood copper Liver copper
Kid number (umo1/1) (pg/g dw)
30

1 ND 1

20
4 ND 6 20

9 3 4
10 3 6 10

ND
17
20 ND
2
9 20 40
I 20 40 60 80 100
21 4 < 20' blood copper Imnol/II lIvercopper(0/9 drY weight)

22 7 < 20' Fig. 9. Distribution of blood and liver copper

23 3 9 concentrations of control goats.

ND = not determined a. Blood samples of 35 goats (25 adults and 10 kids).

`: in liver biopsy.
DISCUSSION
The signs and lesions of the goat kids de-
scribed here are identical to those reported
previously (5, 8, 13, 15, 22, 23). The similar-
ity of the lesions with those seen in delayed
swayback in lambs is striking (3). How-
ever, some differences can be noted. Degen-
eration of the ventral spinal nerve roots
and peripheral nerves was conspicuous in
our kids. This was clinically evident by the
observed hypotonia and hyporeflexia and
was substantiated by the electromyogra-
phic findings in 2 cases. The degeneration
Table 3. Blood copper levels of goats present or 3 properties with swayback history.
b. Liver samples of 37 goats (35 adults and 22 kids).
Samples of 7 adult goats with liver copper concen-
trations over 100 pg/g dry weight are not shown.
of the recurrent laryngeal nerve, which
probably caused the respiratory stridor in
one kid would be another expression of
peripheral nervous system involvement.
Degeneration of ventral spinal nerve roots
in goats with swayback has been mention-
ed by other authors (8, 15), but has been
rarely reported in lambs (17). Degenera-
tion of peripheral axons up to the ventral
spinal roots may only reflect a further pro-
gressive stage of the disease, which is
usually not reached in lambs. Long sur-

Blood copper
Property Goat (pmo1/1) Offspring

Afr. dwarf 4 affected twins (No. 8)

Afr. dwarf 3 affected twins (Nos 9 and 10)
Afr.dwarf ND normal twins (blood copper: 3 and 8 pmo1/1)
Afr.dwarf 4 normal single kid (blood copper: 3 pmo1/1)
Afr. dwarf 7 normal single kid (blood copper: 6 pmo1/1)
Afr. dwarf 8 affected single kid (No. 16)
1
Afr. dwarf 4 affected single kid (No. 17)
Afr. dwarf 5 none
Afr. dwarf 2 none
Afr. dwarf 3 affected single kid (No. 23)
Afr. dwarf 9 normal single kid
Afr. dwarf 3 normal single kid .
Afr. dwarf 4 none
Afr. dwarf (male) 15
French alpine 20 normal single kid
French alpine 9 twins (died postnatally)
French alpine 5 twins (died postnatally)
Afr. dwarf cross

THE VETERINARY QUARTERLY, VOL. 8, No. 1, JANUARY 1986 53

 vival times due to individual care as seen in
many of our kids, are more likely in goats
kept on a small scale than in sheep kept in
large flocks.
Cerebellar cortical degeneration and hy-
poplasia, as seen repeatedly by us and also
reported in the literature (5, 8, 14, 15, 16,
19) is another feature which is not com-
monly seen in swayback in lambs. How-
ever, such cerebellar lesions have been re-
ported in lambs as well (2, 14).
Recently cavitation of the cerebral white
matter, a frequent observation in congeni-
tal swayback in lambs, has also been report-
ed in congenital cases in goats (14).
On morphological grounds it thus seems
justified to consider this disease in sheep
and goats as a single nosological entity,
with only minor differences in expression
between the two species.
The selective involvement of certain neu-
ronal populations, especially those having
long processes within the central nervous
system or extending into peripheral nerves,
is in favour of a primary neuraxonal dis-
ease as opposed to a primary myelin dis-
order. The nature of the lesions both at
light and electron microscopic level also
suggests that myelin degradation occurs as
a secondary phenomenon (Wallerian type
degeneration). It has been suggested that
the first neuraxonal changes in swayback
take place in the axon (8, 20), causing retro-
grade changes in the nerve cell body. This
view would be consistent with the disper-
sion of granular endoplasmic reticulum as
seen by us, and the fibrillary accumulation
in the nerve cell body observed by others
(6). Similar changes may occur in the nerve
cell body after experimental axotomy, in
neurons that regenerate as well as in those
that ultimately die (24). The neuronal ne-
crosis, phagocytosis and loss observed in
our material indicate that irreversible
changes often occur. Proximal axonal
swellings filled with neurofilaments may
reflect an impaired axonal transport of cy-
toskeletal proteins (12). such impairment
might be related to a deficient energy sup-
ply, due to decreased activity of the copper
containing enzyme cytochrome oxidase, as
has been demonstrated in motor neurons
in swayback in sheep (11) and goats (16).
54
Cerebellar cortical dysplasia, as seen in
some kids, has also been observed in experi-
mental copper deficiency in guinea pigs
(10), and in Menkes kinky hair disease, a
hereditary disorder associated with low tis-
sue copper levels in man (9).
Our data from the copper analyses support
an aetiological role of copper deficiency in
swayback in goats. Statistical analysis
showed that the available blood and liver
copper levels of affected kids, their dams
and other herd mates were significantly
lower than those of random control goats.
Moreover a favourable effect was observed
after copper supplementation in some in-
stances. However, since equally low copper
levels were found in kids with and without
nervous signs, it could be postulated that
unidentified factors in addition to copper
deficiency are necessary to induce nervous
disease. Such a multifactorial aetiology has
also beet) suggested for a swayback-like
disease in red deer (27). A possible role of
vitamin A deficiency in addition to copper
deficiency has been discussed (16).
The low liver copper values in a relatively
high percentage of our control goats, espe-
cially in immature animals, would indicate
that low copper status is not uncommon in
Dutch goats. Since many of these kids had
died spontaneously it cannot be excluded
that death was partly attributable to copper
deficiency.
The cause of the low copper status in the
ataxic kids is not known. A primary copper
deficiency cannot be excluded. The copper
requirements of goats are often assumed to
be similar to those of sheep (28). However,
since goats have a lower capacity of hepatic
storage of copper (21), it could be postulat-
ed that goats need a higher daily intake of
copper than sheep. Copper supplementa-
tion during gestation has been shown to
improve postnatal growth in African dwarf
goats (1). In several instances in our series,
sheep concentrate, which is low in copper,
had been used as supplementary food, and
on two occasions no further cases of sway-
back occurred after replacement of sheep
concentrate by concentrate for cattle and
horses.
The possibility of a conditioned copper de-
ficiency must be considered, but informa-
tion concerning factors known to reduce
THE VETERINARY QUARTERLY, VOL. 8, No. 1, JANUARY 1986
the availability of copper such as excess of
molybdenum, sulphate and heavy metals
(7) is lacking.
The possibility of a genetic predisposition
of African dwarf goats for copper de-
ficiency must be considered, since African
dwarf goats were overrepresented in our
material. Genetic variation in swayback
incidence and in blood and tissue copper
concentrations have been observed in differ-
ent breeds of sheep (26).
Further research is needed to elucidate the
complex factors involved in copper de-
ficiency, its relationship to swayback in
goats and sheep, and the possible differen-
ces in copper requirement in the two spe-
cies.
ACKNOWLEDGEMENTS
We are indebted to Dr. G. J. Binkhorst for providing
clinical information and for valuable comments on
the manuscript, to Mr. A. van Beek for accurately
carrying out the copper analyses, to Dr. J. J. van Nes,
who performed the electromyographic examinations,
and to Dr. J. E. van Dijk, who kindly supplied ex-
perimental goats for reference copper values.
REFERENCES
I. Ademosun, A. A. and Munyabantu, C. M.
Copper requirements for the West African dwarf
goat. Proceedings of the 3rd international confer-
ence on goat production and disease. Tucson,
Arizona 1982; 560.
2. Barlow, R. M. Further observations on sway-
back. 1. Transitional pathology. J. Comp. Path.
1963; 73: 51-60.
3. Barlow, R. M., Purves, D., Butler, E. J., and
Maclntyre, I. J. Swayback in South-East Scot-
land. II. Clinical, pathological, and biochemical
aspects. J. Comp. Path. 1960; 70: 411-28.
4. Barlow, R. M., Robertson, J. M., Owen, E. C.,
and Proudfoot, R. A condition in the goat re-
sembling swayback in lambs. Vet. Rec. 1962; 74:
737-9.
5. Beust, B. R. von, Vandevelde, M., Tontis, A.,
and Spichtig, M. Enzootische Ataxie beim Zick-
lein in der Schweiz. Schweiz. Arch. Tierheilk.
1983; 125: 345-51.
6. Cancilla, P. A. and Barlow, R. M. Structural
changes of the central nervous system in sway-
back (enzootic ataxia) of lambs. II. Electro-
microscopy of the lower motor neuron. Acta
Neuropathol. 1966; 6: 251-9.
THE VETERINARY QUARTERLY, VOL. 8, No. 1, JANUARY 1986
7. Commonwealth agricultural bureaux: The nu-
trient requirements of ruminant livestock. Chap-
ter 6: Trace elements, Unwin Brothers, The
Gresham Press, Old Woking, Surrey, U.K., 1980.
8. Cordy, D. R. and Knight, H. D. California goats
with a disease resembling enzootic ataxia or
swayback. Vet. Pathol. 1978; 15: 179-85.
9. Crome, L. and Stern, J. In: Greenfield's Neuro-
pathology. Edited by W. Blackwood and J. A.
M. Corsellis. Chapter 12, p. 536. Edward Arnold
Ltd., London, 1976.
10. Everson, G. J., Shrader, R. E., and Wang, T.
Chemical and morphological changes in the
brains of copper-deficient guinea pigs. J. Nutr.
1968; 96: 115-25.
I I. Fell, B. F., Mills, C. F., and Boyne, R. Cyto-
chrome oxidase deficiency in the motor neurones
of copper-deficient lambs: a histochemical study.
Res. Vet. Sci. 1965; 6: 170-7.
12. Griffin, J. W., Hoffman, P. M., Clark, A. W.,
Caroll, P. T., and Price, D. L. Axonal transport
of neurofilament proteins: Impairment by /3, B1-
iminodiproprionitrite. Science 1978; 202: 633-5.
13. Hedger, R. S., Howard, D. A., and Burdin, M. L.
The occurrence in goats and sheep in Kenya of a
disease closely similar to sway-back. Vet. Rec.
1964; 76: 493-7.
14. Howell, J. McC., Pass, D. A., and Terlecki, S.
Swayback lesions and vulnerable periods of de-
velopment. Proceedings of the 4th international
symposium on trace element metabolism in man
and animals. Perth, Western Australia, 11-15
May 1981. J. M. Gawthorne, J. McC Howell,
and C. L. White, Editors. Springer-Verlag. Ber-
lin Heidelberg New York 1982; 298-301.
15. O'Sullivan, B. M. Enzootic ataxia in goat kids.
Austr. Vet. J. 1977; 53: 455-6.
16. Owen, E. C., Proudfoot, R., Robertson, J. M.,
Barlow, R. M., Butler, E. J., and Smith, B. S. W.
Pathological and biochemical studies of an out-
break of swayback in goats. J. Comp. Path. 1965;
75: 241-51.
17. Palmer, A. C. Nervous diseases in animals. The
Veterinary Annual 1968; 9: 178-84.
18. Pekelder, J. J. Kopergebrek en swayback bij
lammeren van schaap en geit. Tijdschr. Dierge-
neeskd. 1982; 107: 93-6.
19. Seaman, J. T. and Hartley, W. J. Congenital
copper deficiency in goats. Austr. Vet. J. 1981;
57: 355-6.
20. Smith, R. M., Fraser, F. J., and Robertson, J. S.
Enzootic ataxia in lambs: absence of detectable
neuronal pathology in foetal and neonatal spinal
cord. J. Comp. Path. 1978; 88: 401-8.
21. Soli, N. E. and Froslie, A. Copper, zinc and
molybdenum in goat liver. Acta Vet. Scand.
1979; 20: 45-50,
22. Summers, B. A., Appel, M. J. G., Greisen, H. A.,
Ebel, J. G. Jr., and Lahunta, A. de. Studies on
viral leukoencephalomyelitis and swayback in
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23. Taylor, P. A. Enzootic ataxia (swayback) in
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55
 25. Underwood, E. J. Trace elements in human and
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27. Wilson, P. R., Orr, B., and Key, E. L. Enzootic
ataxia in Red deer. N.Z. Vet. J. 1979; 27: 252-4.
28. Winter, J. and Gorsch, R. Ziegen als Versuch-
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Versuchstierk. 1974; 16: 256-65.

Ototoxicity of the antiseptic combination

chlorhexidine/cetrimide (Savlon®):
effects on equilibrium and hearing
H. G. Gall& and A. J. Venker-van Haagen2

SUMMARY Literature concerning the ototoxicity of the antiseptic combination chlorhexidine/cetri-

mide (Savlon8) is reviewed The ototoxic effects are illustrated by the results of our own experiments in
guinea pigs. The impetus for this article was the observation of vestibular dysfunction in 15 clinical
cases (12 dogs and 3 cats), in 8 of which it was confirmed that the ear canal had been rinsed with this
drug combination in the presence of a ruptured tympanic membrane.

Rinsing of the external ear canal is the
principal treatment of otitis externa in
dogs. Preferably this is carried out with
water or saline; the Ilse of antiseptics is not
recommended because the tympanic mem-
brane may be perforated and as a conse-
quence the antiseptic may damage the lab-
yrinth (19). Nevertheless, in some practices
it is customary to use antiseptic fluids for
rinsing the ear canal, which may give rise to
complications.
Between 1975 and 1980 twelve dogs and
three cats were referred to the Utrecht Uni-
versity Small Animal Clinic with equi-
librium disturbances which had developed
shortly after ear treatment by the veterin-
ary practitioner. In most cases the animal
had been treated under anesthesia and the
signs of equilibrium dysfunction had be-
come evident upon arousal. Full details of
the treatment procedure were not always
provided, but in eight of the cases chlor-
hexidine/cetrimide3 had been used to rinse
the external auditory canal.
On admission all animals had the classical
signs of unilateral vestibular dysfunction
and the tympanic membrane on the affect-
ed side was found to be perforated. The
severity of the signs of vestibular dysfunc-
tion decreased with the length of time be-
tween onset and admission. In all cases
there had been eye nystagmus, falling to
one side and tilting of the head toward the

' Department of Otorhinolaryngology, University Hospital, State University of Utrecht. Catharijnesingel 101,
Utrecht, The Netherlands.
2 Small Animal Clinic, State University of Utrecht, Yalelaan 8, Utrecht, The Netherlands.
3 Savlon®, I.C.I., Rotterdam, The Netherlands.

56 THE VETERINARY QUARTERLY, VOL. 8, No. I, JANUARY 1986