J. COMPo PATH. 1962. VOL. 72.

SOME CLINICAL AND EXPERIMENTAL OBSERVATIONS

ON NATURALLY-OCCURRING PANTOTHENIC-ACID
DEFICIENCY IN PIGS
By
R. F. W. GOODWIN
Department qf Clinical Studies, Universi!y of Cambridl!.e
INTRODUCTION
Pantothenic-acid deficiency in the pig has been studied experi-
mentally for a number of years but, as with other vitamin defici-
encies, the earlier work was handicapped by uncertainty concerning
the true nature of the deficiency states observed.
Briggs and Daft (1954) concluded that, even as late as 1941, the
deficiency signs produced by experimental diets could have been due
to a shortage of other factors in addition to an insufficiency of pantothenic
acid, but from subsequent work, involving more complete diets, they felt
that they could safely list the gross clinical and pathological signs of the
experimental disease.
Reports of the naturally-occurring disease, such as that of Schulze
(1960) , have been few and, as might be expected, they have not
approached the standard of the experimental observations in defining
the condition being described. Doyle (1937) encountered a condition
that might have been pantothenic-acid deficiency, but he favoured an
infective aetiology. Hughes (1942) stated that goose-stepping in pigs had
been reported "from many sections of the country" (U.S.A.), and Hughes,
Crampton, Ellis and Loeffel (1944) suggested that "the frequent occur-
rence of 'goose-stepping' in farm swine herds may be evidence of a
pantothenic-acid deficiency".
The availability of a large herd of pigs, apparently suffering
from pantothenic-acid deficiency, and at the same time free of
enzootic pneumonia (which otherwise might have interfered seriously
with controlled nutritional trials), provided the writer with a very
favourable opportunity to study this deficiency disease under field
conditions. Once the presence of the disease had been established
in this herd, other herds were investigated and some wider con-
clusions were drawn on the influences that might now be governing
the pattern of the field disease. The account that follows appears to
be the first report of pantothenic-acid deficiency in British pigs.
METHOD
To estimate the pantothenic-acid content of meals, 5 g. samples of
meal were shaken with 500 ml. of phosphate buffer solution (pH66) at
5 min. intervals during half an hour. The extract was then filtered,
diluted, and assayed with Lactobacillus arabinosus againt a calcium D-
pantothenate standard. The results obtained, therefore, have been
related to calcium pantothenate, rather than pantothenic acid.
R. F. W. GOODWIN
RESULTS
HERDQ
General History
21
5
This herd of pedigree Landrace pigs comprised about 40 breed-
ing females and their offspring, the latter being fattened for bacon
production. It had been apparently free of enzootic pneumonia
for some years and by 1960 had fully complied with the standards
of the Association for the Advancement of Virus Pneumonia Free
Pigs*.
The first signs of the disease that is more fully described later
appeared in a litter born in December, 1957: the whole litter showed
varying degrees of weakness in the hind legs, associated with scouring
and unthriftiness, before weaning. A few other litters were similarly
affected during 1958, and by January, 1959, a litter born in the
previous October had become severely affected: the scouring which
had been present before weaning, was now bloodstained; there was
also anorexia and marked posterior weakness, and one animal had
died. The number of clinical cases decreased during the next 4
months, but by June, I959, it appeared that the disease was becom-
ing both more common in the growing pigs and more severe, in that
the litters were now showing clinical signs at a younger age. Thus,
a litter born in mid-May was scouring by 6 days of age and showing
posterior weakness when just over 2 weeks old. In July, 126 pigs
over weaning age were examined: of these, 49 were obviously
affected neurologically, and 6 more might have been showing early
signs-an incidence based on neurological involvement alone of
nearly 50 per cent.
As the pig is not an easy subject for detailed clinical examination,
particularly when neurological signs are being recorded, all tests in
which the animal's response was questionable have been omitted.
The essential clinical features of the disease, however, were as
follows.
Clinical Signs in Weaned Pigs
Although the scour rarely became extremely watery, some
fluidity of the faeces was common, and this usually preceded other
signs. One of the earliest neurological signs was difficult to detect,
as it was merely a slightly faulty action of the hind legs, including a
mincing gait or a somewhat stiffer movement than is usual. Slight
abnormalities of this type are sometimes seen in pigs, particularly
Landrace animals, on diets not deficient in the B-group vitamins.
When the disease did not progress beyond this stage, therefore, it
could not be certain that some hereditary factor was not involved.
Many cases that were first diagnosed in this way, however, pro-
ceeded to advanced posterior inco-ordination. Another mild sign was
* See Goodwin and Whittlestone (1960) for the nomenclature used in respiratory
diseases, and for the regulations and standards of the Association.
216 PANTOTHENIC-ACID DEFICIENCY IN PIGS
muscular tremor over the hind quarters when standing still. In
several other animals, one of the earliest signs was a slight snatching
movement in the hind legs on walking but, as pigs normally move
with a slightly stilted hind-leg action compared with other species,
the first signs of abnormality were, once again, not always clear-cut.
One of the next stages in the condition was swaying of the hind
quarters. Some pigs so affected stood with their hind legs slightly
more apart than usual, and a few showed a dip in the back at the
lumbar region.
Thereafter, the clinical signs were more obvious, but in referring
to them it should be remembered that, in such a large number of
affected animals, there were many intermediate variations in the
present set descriptions. In the main, the abnormalities of movement
fell into 2 groups: first, exaggerated actions with the hind legs and,
secondly, progressive paralysis of the hind legs. The exaggerated
action usually commenced as a slight snatch as the hind feet left the
ground. This became progressively more marked and was com-
monlyassociated with a forward-reaching movement of the leg as
the feet returned to the ground. The combination of a very high
lift of the hind leg with the reaching forward under the abdomen
produced the so-called "goose-stepping" movement (Figs. I, 2, 3
and 4). In several cases this action became so great that the hock
joint approached the ground (Fig. 8); this necessitated a lowering
of the pelvis. Pigs thus affected often moved quite rapidly with a
peculiar waddling, rolling, duck-like action. It was observed that
some of the animals that goose-stepped when moving, periodically
snatched their hind legs from the ground when standing still (Fig. 6).
Behaviour similar to this was observed by Hughes and Ittner (1942)
and Colby, Cunha, Lindley, Cordy and Ensminger (1948) in the
experimentally-produced disease.
When the signs were largely of the second type, the earlier sway-
ing action advanced to marked inco-ordination (Figs. 10 and 1 I),
the hind quarters often collapsing to one side. On a slippery surface,
this collapse was more frequent, the hind legs commonly being
splayed out anteriorly on the ground (Fig. 12). Fairly advanced
cases of this type could not raise their hind quarters from the
ground unaided (Fig. 10), but they could sometimes stand once they
had been assisted to that position. In the most advanced cases, the
hind legs were incapable of supporting the body; pigs thus affected
often propped themselves up on their forelegs and sat with both
hind legs to one side. Nearly all such cases managed to move about
fairly well, and no case became immobile. The only animal with any
involvement of the forelegs showed a completely atypical movement
(see later, test I), and at post-mortem examination an abscess was
found in the cervical vertebrae; it is probable, therefore, that this
case was unrelated to the main problem. Occasionally, however,
the forelegs became distorted and the carpal joint more flexed, as a
consequence of a long-standing grossly abnormal posterior gait
R. F. W. GOODWIN 21
7
(Fig. 9). Wintrobe, Miller and Lisco (1940) reported that some of
their experimental cases were affected in the forelegs, but they gave
little further information on the clinical nature of the abnormality.
Some of the pigs that dragged their hind legs, protested violently
and withdrew the appropriate limb sharply when a needle was
stabbed into the skin near the coronet. Other such cases, however,
responded sluggishly to this test, while a few others showed no
reaction at all, not even an awareness that the test was being per-
formed. These latter cases, like all the other affected animals,
never developed a totally flaccid paralysis; whether any increased
tone was present in these animals was difficult to determine.
The various abnormalities described above did not necessarily
follow in a set sequence. Furthermore, the disease could become
clinically arrested at any point. Thus, many animals never progressed
beyond the milder stages, even though they remained on the same
diet for many weeks after showing their severest signs. No definite
instance of improvement was seen by the author, although the owner
believed that 2 pigs went off their hind legs for a week or so, but
later walked again with difficulty. Many of the severely-affected
animals remained in surprisingly good condition; they rarely had
the bloom of normal pigs but, by dragging themselves to feed, they
managed to grow and keep reasonably well-fleshed. This was not
always so, however, as several pigs lost condition and developed a
wrinkled skin which, on occasions, was a slightly-yellow colour.
The above clinical signs were suggestive of pantothenic-acid
deficiency. Before describing the investigation of this probability,
however, it is convenient to mention briefly the effects of the disease
in sows and young litters.
Clinical Signs in Sows and Young Pigs
The sows themselves remained free of clinical signs. However,
the owner believed that, in addition to the obvious scouring and
checking in growth that commonly developed after a few weeks, the
litters were becoming increasingly less viable at birth.
Another sign of note in young pigs was a characteristic loss of
hair. As the growth of many litters was retarded, the hair was often
longer than usual. The areas of baldness, therefore, which were
first seen between the ears and on the nape of the neck, were all the
more striking; thereafter, the baldness spread rapidly down the
spine, and then outwards over the ribs and flanks. A similar dis-
tribution of the alopecia in experimentally-produced cases has been
noted by Hughes and Ittner (1942), Wintrobe, Miller, Follis, Stein,
Mushatt and Humphreys (1942), Wintrobe, Follis, Alcayaga,
Paulson and Humphreys (1943), Moustgaard and Thorbek (1949)
and Wiese, Lehrer, Moore, Pahnish and Hartwell (1951). This
phase was followed by one of new hair-growth, in which the pigs had
an unusual appearance, because much of the skin, notably on the an-
terior part of the body, was covered with a fine, short stubble (Fig. 13).
218 PANTOTHENIC-ACID DEFICIENCY IN PIGS
Pathological Findings
Only two aspects of the laboratory examinations will be mentioned
here. First, haematological observations on a few advanced neuro-
logical cases in fattening pigs revealed no noteworthy degree of
anaemia. Secondly, the main gross lesions seen post mortem were
in the alimentary tract. In early cases there was a catarrhal
enteritis; longer-standing cases often showed a necrotic enteritis or
thickening of the lower ileum (Figs. 15, 16 and 17). Not infrequently
there were varying degrees of gastritis (Fig. 14), and occasionally
these alimentary changes were complicated by peritonitis or bowel
rupture.
Nutritional Investigations
The Diet
All the pigs on the farm had been fed home-mixed rations of
constant composition since about mid-1956 (Table 1). It is relevant
to record that the owner had been advised that these diets would be
adequate, a point that will be returned to in the discussion. The
No. 1 ration was fed, after a short period of creep-pellet feeding,
until the pigs reached about 120 lb. liveweight; the No.2 ration was
fed thereafter until slaughter. To all three rations, a supplement of
vitamins A and D
3
, a mineral supplement, and a vitamin B12 sup-
plement were added, according to the manufacturer's instructions.
TABLE I
RATIONS FED IN HERD Q
Constituent
l _ s ~
No. I NO.2
Barley meal
6 I
6 6
Ground wheat .. 2
I
2
Sharps (fine to medium bran)
White fish meal
!
a
"
Soya bean meal
1
! t 1!"
Bean meal
t ! !
A sample of the No. 1 meal was collected at the beginning of the
investigation and a further sample in late October, 1959. Both
were analysed for pantothenate: they agreed closely in their content,
and yielded a maximum of about 2'25 mg.jlb. of food (5/Lg.jg.).
A sow-and-weaner meal, made up with a proprietary concentrate-
balancer, was analysed at the same time, and this yielded just over
5 mg.jlb. of meal (11 3/Lg.jg.). Almost a year later (in August, 1960),
the farm-mixed meal was sampled again and analysed by the same
method. The agreement on parallel samples showed a greater
variation, due perhaps to inadequate mixing on the farm, but the
R. F. W. GOODWIN 21
9
mean of 2 mg. jIb. (4'5 fLg.jg.) was not very different from the
earlier analyses. The sample of farm-mixed meal collected in
October, 1959, had been kept and this was re-analysed, as also was
a meal made with the same proprietary concentrate referred to
earlier: the results were similar to those of the previous year.
Prophylactic Supplementation with Calcium Pantothenate
The simplest way to confirm the suspected aetiology was to
supplement the diet with the pure vitamin under controlled condi-
tions. All the 4 tests described below were made on the farm in the
normal fattening pens. Apart from the prophylactic supplements,
the management was unaltered.
Supplementation after weaning (Test I). This test began on January
29th, 1960. Each of 3 litters was divided between groups A and B.
Group B received the basic diet; group A received in addition 20 g.
calcium pantothenate/t ton of meal for the first week, and IO g.
calcium pantothenatej! ton of meal thereafter. Table 2 summarizes
the results. In all the 4 tests of this type the pigs were killed at
about 200 lb. liveweight unless they had become casualties earlier.
As both groups continued to scour after weaning, it seemed
probable that the deficiency was already developing in utero or
during suckling. To reduce this variable in future tests, without
recourse to supplementing the sow's diet, those animals in each
litter earmarked to receive the fortified ration after weaning were
injected intramuscularly with 12 5 mg. of panthenol * every other
day.
TABLE 2
PANTOTHENATE SUPPLEMENTATION AFTER WEANING IN HERD Q
Animals Animals developing
Group starting test Scouring neurological signs
A
11* Persisted for 1**
6 weeks
B 12 Persisted for
5t
(Controls) 6 weeks
I
* Reduced to 8 by fortuitous causes during the first 6 weeks.
* * This animal had an abnormal gait after 12 weeks; the forelegs were involved and
post-mortem examination revealed an abscess extending into the lower cervical vertebrae.
t Swaying of hind quarters, goose-stepping and difficulty in standing.
Panthenol injections bifore weaning (Test 2). This test began on
March 3rd. Two litters of 9 pigs each were divided and cross-mixed.
Those animals going into group A received their first panthenol
injections at 4 to 5 weeks of age. From 8 weeks of age, the latter
group received a calcium pantothenate supplement at the rate of
IO g.!! ton of meal. Table 3 summarizes the results.
* Bepanthen : Roche.
220
PANTOTHENIC-ACID DEFICIENCY IN PIGS
TABLE 3
PANTHENOL INJECTIONS BEFORE WEANING IN HERD Q
Animals Animals developing
Group starting test Scouring neurological signs

A
st
None 0
B 10 Marked
5*
(Controls)
t One pig died suddenly after 7t weeks.
* A sixth pig was probably an early case. Four of these 5 cases were litter-mates,
indicating that the 2 litters had been differently conditioned before 4 weeks of age,
probably by the nutritional status of their dams.
Panthenol injections soon after birth (Tests 3 and 4). Test 3 began on
April 7th. Because of the need to mix litters of comparable size,
only 15 pigs were available in 2 litters. Group A received panthenol
injections from the first week of life and a supplement of calcium
pantothenate at IO g./! ton of meal when going on test after weaning.
None of the 7 animals in group A scoured or developed neuro-
logical signs. No neurological signs appeared in the 8 controls, but
this group scoured for about a month after weaning. In this test,
therefore, there was little over-all difference between the 2 groups.
This could not be explained by a difference in maternal diet; for
although many sows on the farm were now receiving a fortified
ration during pregnancy, both the dams of these litters had contin-
ued on the unfortified ration.
Test 4 was a repeat of test 3. Three litters of 9, 10 and 7 pigs,
were split between groups A and B (13 pigs in each group). They
were weaned on May r rth, those animals going into group A having
had panthenol injections thrice-weekly from the first week of life.
Due to a mistake, group A received 2t per cent dried yeast, in
addition to the above supplement of calcium pantothenate, for the
first 20 days of the test; thereafter, the yeast was omitted. All the
dams were fed the unfortified ration throughout pregnancy.
In neither group did neurological signs appear. Group A scoured
a little, but the controls scoured severely for at least 6 weeks.
Other Observations Relating to Herd Q,
Attempts at Therapy
Until the controlled tests just described could be organized, the
many affected animals in herd Q provided an opportunity to
ascertain whether any amelioration of the clinical signs could be
initiated by a change in diet. Neurologically, there was little hope
of such an improvement, but it seemed worthwhile to confirm this
and, at the same time, observe any other effects of treatment.
R. F. W. GOODWIN 221
The farm was visited on August 1st, 1959, and 9 pens of pigs
were selected in which the animals were not yet close to slaughter
weight. Each pig in these pens was examined and the degree and
type of clinical affection recorded. In all, there were 79 pigs, of
which 55 were showing neurological signs. A total of 32 pigs, of
which 27 were affected neurologically, then had their basic diet
fortified with 2 per cent dried yeast; a further 41 pigs, of which 28
were affected neurologically, had their diet fortified with calcium
pantothenate-to give each pig a total daily intake of about 200 mg.
of the vitamin; a pen of 6 pigs, all of which were at that time un-
affected neurologically, continued on the basic diet unchanged.
The improved diets were first fed on August 3rd, and 46 days later
all the pigs were again clinically examined.
In the group receiving yeast, one animal was definitely worse and
2 animals appeared to be less affected; otherwise, there was very
little change neurologically. The scouring in this group, however,
was less marked. Of those receiving calcium pantothenate, 5 seemed
definitely worse, 2 were rather better, and the remainder were much
the same neurologically; again, however, the scouring was noticeably
better. The control group of 6 pigs had shown only some scouring
at the first examination; 4 of the 5 animals remaining alive, however,
now showed definite neurological signs. In the main, therefore,
there was little change in the degree of neurological involvement,
once the diet had been fortified with either yeast or calcium panto-
thenate; on balance, perhaps, a slight deterioration had occurred.
During the same period, however, nearly all the animals in the
small untreated group had obviously worsened. These results are
more in keeping with those of Wintrobe et al. (1943), who checked
the scouring but obtained only some improvement of the ataxia on
treating experimentally-produced cases, than of Wiese et al. (195 I),
who implied that high doses of calcium pantothenate produced a
complete recovery in very young pigs.
Feeding Experiments in a Different Environment
In parallel with the last experiment, and again until such time
as the more precise diagnostic experiments were undertaken on the
farm, some feeding experiments were carried out in Cambridge.
Fifteen weaners from 2 litters born in an experimental herd in
Cambridge were fed on the basic diet that was being mixed on the
farm. The experimental herd supplying the 2 litters was chronically
infected with enzootic pneumonia and, as a result, the average rate
of growth of the fattening pigs in this herd was slower than in herd
Q. Another difference was that the 15 weaners were not Landrace
pigs and, furthermore, they were born from sows that had been fed
a meal during pregnancy made up with the proprietary concentrated-
balancer referred to earlier. Eleven pigs went to slaughter after
being on the unfortified (herd Q) diet for 4t months, and the
remaining 4 pigs went a month later. Throughout this time all 15
222 PANTOTHENIC-ACID DEFICIENCY IN PIGS
animals appeared completely normal, ate well and had very firm
dung. The disease was not readily reproducible, therefore, when the
same diet was fed to weaners in another herd.
The second main feeding experiment in Cambridge was with
weaners moved from the affected farm. A total of 25 pigs, 14 being
8 weeks old and I I being 7 weeks old, was split into 2 groups of 13
and 12; the first group was fed the basic, herd Q ration (mixed on
the farm) and the second group was fed an identical ration, but
with dried brewer's yeast added at the rate of 2 lb. per I 12 lb. *
Unfortunately, it was not possible to house these 25 pigs in complete
isolation; instead, they went into 4 rooms opening into a central
corridor, with the 15 pigs probably infected with enzootic pneu-
monia, mentioned above, in 2 nearby rooms opening into the same
corridor. It seemed but a question of time, therefore, before the
imported weaners contracted enzootic pneumonia.
Three to 4 weeks after the experiment started, both groups of
weaners from herd Q developed profuse diarrhoea, associated with
pyrexia; 2 pigs died in the group receiving yeast, leaving IO to
finish the test, and 4 pigs died in the group without yeast, leaving 9
to finish the test. The exact cause of this trouble was not clear, and
it could well have been due to a combination of a deficiency state
with the onset of enzootic pneumonia; both groups were coughing
some weeks later. Once the crisis had passed, however, the group
receiving yeast continued well; there was no further scouring and
no neurological involvement at any time. In the group not receiving
yeast, however, 3 out of the 9 survivors developed neurological
signs: these first appeared after 9t weeks, and eventually consisted
of a swaying gait in one animal, a high-stepping walk in a second
and an inability to stand on the hind legs unaided in the third. The
test lasted for 20t weeks, when all the survivors were slaughtered.
It thus appeared that not only were neurological signs prevented
by a low level of dried brewer's yeast in the ration, but that a check
in growth rate might reduce the severity of the clinical disease (see
Discussion) .
Subsequent Events
During 1960, apart from those in-pig sows whose litters were to
be used for the controlled trials above, the herd was gradually
changed over to a supplemented ration. At first, the supplement was
dried yeast, but this was later replaced by a multiple vitamin-B
mixture. Thereafter, no further neurological evidence of panto-
thenic-acid deficiency was seen, and the average rate of growth was
satisfactory. This can be shown by the growth rate of the litters that
entered the fattening pens after the beginning of test 4. During May
and June, 1960, a total of 67 pigs that were not required for any
* Yeast was used because it was not then known that pantothenate alone would
prevent the condition. The rate of yeast supplementation was low, but such a supple-
mented diet would, theoretically, supply about 25 per cent more pantothenate than the
unfortified ration.
R. F. W. GOODWIN
223
test were weaned and fattened under normal conditions; 65 of these
reached bacon weight. The exceptions were a pig that died shortly
after weaning, and a very small weaner that was slaughtered at a
lighter weight because it lagged behind its litter-mates. Figures are
available for 61 of the bacon pigs: the average dead-weight was
157 lb. at an average age of 175 days.
Because it seemed probable that the deficiency condition in
herd Q was partly related to the high average rate of growth of the
fattening pigs, compared with most pig herds, a number of other
herds, also free of enzootic pneumonia, were examined to see whether
they too showed any signs ofpanthothenic-acid deficiency. Three out
of the 9 herds examined somewhat superficially contained pigs that
appeared to be so affected clinically. In the first herd (herd N)
there was swaying of the hindquarters in some young litters and a
number of cases of slight snatching of the hind legs among the older
pigs in the fattening house. Herd N also contained Large White pigs
that were housed and fed exactly as were the Landrace; none of the
~ r g e white animals developed neurological signs of pantothenic-
acid deficiency.
In 2 other herds (MG and DO), the main sign was posterior
weakness, the affected fattening pigs subsequently losing the use of
their hind legs.
All the 3 affected herds consisted entirely (MG and DO) or
largely (N) of purebred Landrace pigs, like herd Q, and all were
likewise being fed on home-mixed rations; they all also had an
average rate of growth very similar to that in herd Q.
TABLE 4
RATIONS FED IN HERDS N, MG AND DO
Constituent HerdN Herd MG Herd DO
Barley meal
. . 3
8 II
14
Wheat meal
. .
25
6
4
Molassine meal
.
.. - I -
White fish meal
.
.. 6 I
It
Soya bean meal
. .
- It
i
Maize meal
. .
25
- -
Groundnut meal .. .. 6 - -
Grass meal
.
..
-
-
t
All 3 rations contained a mineral supplement. In herds MG and DO, vitamins A,
Da and B2 were added, but in herd N, only vitamins A and D3 were incorporated, and
then only in the winter months. In herd N, pigs over about 100 lb. in weight were fed
the same ration as the younger animals, except that the fish meal was reduced to 2t
parts and the groundnut meal increased in compensation.
H
224
PANTOTHENIC-ACID DEFICIENCY IN PIGS
The ration being fed in each herd is shown below (Table 4).
Herd MG was of special interest, because the suckling and fattening
pigs had suffered severely from widespread parasitism, which had
resulted in a poor over-all growth rate; steps were then taken to
prevent the development of parasitism, and the time taken to reach
bacon weight improved strikingly. In parallel with this removal of
the burden of parasitism, the clinical cases of nutritional deficiency
arose.
A clinical pattern was emerging, therefore, of pantothenic-acid
deficiency on home-mixed rations and where the rate of growth of
the fattening pigs was above average. This was not always so, how-
ever; for the disease was subsequently seen in other herds where the
average rate of growth was more conventional.
HERD /0
One of these herds (10) was of particular interest. It consisted
of about 60 Wessex sows and produced either purebred Wessex
litters or first-cross WessexJLandrace litters, mainly for heavy-hog
production. The litters were farrowed in huts at pasture and, when
about 3 weeks old, they were moved with their dams to fenced
paddocks. The herd was almost certainly chronically infected with
enzootic pneumonia, although complete observations were not made
to establish this fact.
For many years the general feeding policy had been to incorpor-
ate a high percentage of waste products in the home-mixed ration.
Thus from 1953 to 1956, biscuit crumbs formed about 20 to 25 per
cent of the diet. At the end of 1956, a year's supply of dried potatoes
TABLE 5
RATIONS FED IN HERD 10
Constituent Suckling pigs Weaners
(to I6 weeks)
Fattening pigs Sows
Biscuit-wafer meal 2 Ii
I
i
Bread-crust crumbs
4 3 4 3
Middlings I 2 2 Ii
Barley meal 10 10 II II
Soya bean meal I I
-
I
White fish meal
Ii Ii
I
Ii
Mollassine meal - I I I
Grass meal -
i i
-
All 4 rations were supplemented with a mineral mixture and vitamins A, D3 and B ..
except for the fattening ration, where the vitamin A was omitted.
R. F. W . GOODWIN
225
was purchased as a substitute and, when this was exhausted, a
reversion was made to biscuit-wafer meal, to which bread-crust
crumbs were then added. From early 1958, the rations varied
slightly from time to time, but they were broadly of the pattern
shown in the specific examples (Table 5). During the winters of
1956/57 and 1957/58 a multiple vitamin-B supplement was added,
to supply 25 g. of pantothenic acid per ton of meal. No such
supplement was added again until April, 196 I.
An economic problem became obvious in 1960. Before this date,
the situation had been acceptable, an average of 93 pigs being
reared from 125 litters during the year ending on September 30th,
1958, and 87 reared from 132 litters during the year ending on the
same date in 1959. In the spring of 1960, however, the suckling
pigs seemed less vigorous and when these litters came into the
fattening yards after weaning they progressively worsened: scouring
became widespread and serious, and many animals developed a
goose-stepping gait; some lost the use of their hind legs. By October,
1960, a crisis had developed: many fattening pigs died or had to be
sent for casualty slaughter, and the state of the new-born litters
augured ill for the future. Thus, the average number of pigs per
litter born alive during the year ending on September 30th, 1960
(130 litters) was 7.81, compared with 945 for the previous year
(132 litters); and this figure dropped to 7.36 for 80 litters born
between September 30th, 1960, and April 13th, 1961, resulting in
an average of only 6 weaned. In the 4 months between mid-
December, 1960, and mid-April, 1961, 46 litters were born;
although, as has been shown above, these litters were, on average,
small in numbers, 142 pigs were either born dead or died shortly
after birth-an average of just over 3 per litter. Unfortunately, the
records in this herd did not distinguish between stillbirths and early
neonatal losses at this date. It may be significant that during the
winter of 1960/61, the coughing among the fattening pigs became
very severe and almost universal.
The writer was consulted in March, 1961, and the farm was
first visited at the end of that month. The litters running at pasture
showed a marked incidence of scouring; often the pigs were long-
haired and unthrifty. In several litters, aged 3 weeks and upwards,
pigs were found that were losing their hair, usually starting between
the ears and at the back of the neck, as in herd Q. It was said that
this progressive baldness in litters had been associated with the
development of partial paralysis of the hind legs at about 3 weeks of
age. Groups of weaners running in a wood were examined: several
of these showed similar degrees of baldness and varying degrees of
faulty hind-leg action; coughing was particularly severe in these
litters. Chronic scouring was common among the older fattening
pigs in yards, and a number of the pigs approaching bacon weight
showed a snatching or slight goose-stepping gait with the hind legs.
A clinical diagnosis of pantothenic-acid deficiency was made, but as
PANTOTHENIC-ACID DEFICIENCY IN PIGS
the herd was already suffering severely and was uneconomic, and as
the presence of another chronic disease would probably have made
the interpretation of controlled trials (using pantothenate) difficult,
the diet was fortified on a wider basis at once. Wheat and barley
were substituted for the bread-crust crumbs and biscuit-wafer meal
in all but the fattening ration immediately, and a multiple vitamin
mixture was incorporated in all the rations at the rate of 28 lb. per
ton. The manufacturer's analysis of the vitamin supplement is shown
in Table 6: this is the same supplement as used in the winters of
1956/57 and 1957/58. All the herd was receiving the new formula-
tions by about April 1st.
Although the diet had now been improved, sufficient quantities
of the previous constitutents remained to make up small samples of
meal similar to the rations being fed on the farm earlier in 1961
(Table 5). These were analysed for their pantothenate content by
the same method as before. The sow mix yielded 3.6 fLg.jg. (1.6
mg. jIb. ); the weaner mix yielded 4.0 fLg.jg. (1.8 mg. jIb. ); and the
fattening mix yielded 3.0 fLg.jg. (1'4 mg.jlb.). These figures, rang-
ing from 3'0 to 4.0 fLg.jg. were notably lower than the figure of 5.0
fLg.jg. obtained with the fattening mix being fed at the height of the
trouble in herd Q.
The dietary improvements just described were followed by a
progressive disappearance of those clinical signs specifically
associated with pantothenic-acid deficiency, and there was a con-
commitant marked increase in the general economic efficiency of the
herd.
TABLE 6
VITAMIN SUPPLEMENT USED IN HERD 10
Constituent Vitamins per II!! lb.
Thiamin 224 mg.
Riboflavin 6000 mg.
Pyridoxine 560 mg.
Vitamin B12 1000 mcgm.
Nicotinic acid 28000 mg.
Pantothenic acid 10000 mg.
Vitamin E 2000 LV.
Vitamin K
3350 mg.
Choline 179200 mg.
R. F. W. GOODWIN
227
DISCUSSION
In herd Q, the development of neurological signs in the fatten-
ing pigs was completely prevented, under the controlled conditions
in tests I and 2, by adding only calcium pantothenate to the ration.
Taking these 2 tests together, no neurological signs referable to
pantothenic-acid deficiency occurred among the 15 surviving
animals receiving calcium pantothenate, whereas at least IO
neurological cases occurred among the 22 controls. This fact,
coupled with the analytical evidence that the unfortified ration was
somewhat low in this vitamin, suggests that the main cause of the
disease condition was an inadequate dietary intake of pantothenic
acid. Whether any other deficiency states were contributing to the
clinical picture concurrently is not known, but it is clear that they
were of no great importance; for, although scouring continued in
the first test group being fed the fortified ration, it was possible
largely to prevent this scouring if the vitamin supplement were
given soon after birth (tests 2, 3 and 4).
The ration fed in herd Q was not particularly abnormal. It had
not been criticized by nutritional advisers to whom it had been
submitted and it was probably superior to the very crude rations
associated with nutritional enteritis in the U.S.A. (Luecke, Thorp,
McMillen, Dunne and Stafseth, 1949); many comparable home-
mixed rations must be in use throughout the country. The diet was
inadequate in this instance, however, probably because the average
growth-rate of the fattening pigs was very good. When a herd is
freed of enzootic pneumonia, the most striking results occur at the
fattening stage-the pigs usually growing faster and more evenly
than is customary in infected herds. It might be expected, therefore,
that the first signs of nutritional deficiency would appear in the
growing pigs. The sows and new-born litters, on the other hand,
had no exaggerated dietary demands and as a result, they showed
little clinical abnormality. That the rate of growth after birth was
not the sole factor involved, however, is suggested by the observa-
tion that the litters became affected at a progressively younger age.
Furthermore, the incidence of the disease steadily widened in the
herd, and there was some evidence that litters born from gilts were
more readily affected than those born from sows; these facts point
to an increasing pre-natal/lactational effect with time. Perhaps
the level of pantothenic acid was barely adequate, even for the
adult stock-a situation that would have passed unnoticed had the
growing pigs not been free of chronic respiratory disease. The
feeding tests made in Cambridge, although very limited, support
this general hypothesis. The unfortified ration had no effect on
slower-growing animals born from dams fed a more balanced diet,
while pigs transferred from herd Q and kept in a more diseased
environment did not develop such marked clinical signs as did
comparable and parallel groups kept for a shorter time on the basic
PANTOTHENIC-ACID DEFICIENCY IN PIGS
ration at their home farm. This, therefore, is a different general
situation from that postulated by Luecke, McMillen and Thorp
(1950) in which, by improving the diet without increasing the panto-
thenic-acid level, the growth rate is stimulated to induce a deficiency
state.
It is probable that many pig herds are now on the borderline of
pantothenic-acid deficiency, and that any widespread improvement
in mean growth rates (as are now occurring from a greater apprecia-
tion of the importance of disease control), unless accompanied by a
corresponding compensation in dietary intakes of pantothenic acid,
and perhaps other factors also, could result in economic losses. Pre-
liminary evidence from herds N, MG and DO suggests that a pro-
portion of the herds that are free from enzootic pneumonia have
already moved into the clinical fringe of this particular deficiency.
Apart from improved health standards, however, other factors
appear to favour the development of deficiency signs. The first is
home-mixing of rations. Because it is common among farmers to
fortify pig rations with only riboflavin, among the main group-B
vitamins, the levels of pantothenic acid in pig meals will largely
depend on the nature of the main constituents. Analysis of meals
marketed by 2 large, commercial compounders showed a consider-
ably higher level of pantothenic acid than in the home-mixed ration
of herd Q. However, it is a simple matter to fortify home-mixed
rations with a wider range of group-B vitamins, and any present
advantage in commercially-produced meals in this respect could
readily be equalled on the farm. A second possible factor is variation
in breed susceptibility. Herd Q, as also herds N, MG and DO,
consisted of purebred Landrace pigs, and the disease has not yet
been seen by the writer in Large White herds that are free of
enzootic pneumonia. It is interesting that in herd 10 the farmer
believed that a variable incidence of the disease had occurred; in
effect, most neurological cases were seen in the three-quarter Land-
race pigs, fewer cases occurred in the half-bred Landrace pigs, and
even less in the purebred Wessex litters. Nevertheless, at the height
of the herd trouble, cases of hind-leg weakness were certainly seen
in purebred Wessex pigs, indicating that a sufficiently severe
deficiency of the vitamin must inevitably affect any pig, regardless
of its breed, and even though it is suffering from another disease
that might retard its growth. Breed differences in susceptibility
under experimental conditions, Durocs being more readily affected
than Hampshires, have been reported by Luecke, Thorp, McMillen
and Dunne (1949), and Ullrey, Becker, Terrill and Notzold (1955).
Other, less understood factors might also have been influencing
the over-all incidence of the disease in herd Q. The number of cases
declined in the Spring of 1959, then surged to their greatest impact
during the summer of that year; thereafter, the severity of the neuro-
logical signs appeared to wane-very few animals going right off
their hind legs in 1960. In the last 2 controlled tests (tests 3 and 4,
R. F. W. GOODWIN
229
starting in April and May, 1960, respectively), no neurological cases
appeared in the deficient groups. It is possible, therefore, that this
decline in incidence, occurring at the same time as the decline in
1959, was more than a chance coincidence, and the importance of
the control groups-even in work of this type-is underlined.
Rather more information than is available here would be required
to warrant open speculation on the possible causes of a seasonal
variation in the effects of pantothenic-acid deficiency, but the
simplest explanation, a variation in diet, was partly eliminated by
analysing meal samples taken on 3 widely-spaced dates. These
analyses, however, were made only for pantothenic acid, and inter-
relationships between pantothenic-acid requirements and the levels
of other dietary constituents have been reported under experimental
conditions. Thus protein (Luecke, Hoefer and Thorp, I952), and
chlortetracycline (McKigney, Wallace and Cunha, 1957) appear to
spare pantothenic acid, while biotin (Colby, et at., I94B) and other
additives (Luecke et at., I 950) hasten the appearance of clinical signs.
In herd 10, a somewhat different situation obtained. The dietary
deficiency, as judged by analyses, was more marked, and sufficient
to produce clinical effects even in a herd with an indifferent average
growth rate. Under these circumstances, the deficiency signs might
have been expected to appear throughout the herd, rather than in
one section of it (as in herd Q), and this is what occurred: the
neonatal losses were more severe, and the scouring and hairlessness
among suckling pigs more marked. Compared with herd Q, it is
more probable-because of the waste products in the ration-that
some other deficiency might have contributed to the losses but, even
so, the nature and pattern of the clinical signs strongly suggest that
pantothenic-acid deficiency was the dominant aetiological factor.
Unfortunately, time, distance and the economic state of herd IO did
not allow a detailed study of a succession of new-born litters for the
interesting clinical signs reported by Ullrey, Becker, Terrill and
Notzold (I954, I955). These latter authors (I955), as well as
Hodgskiss, Ensminger, Colby and Cunha (I950) , when studying the
effects of pantothenic-acid deficiency on breeding performance, also
produced clinical signs in adult pigs comparable with those seen in
young growing animals, but in none of the herds mentioned in this
paper were the adults seen to be affected to this degree.
Little need be added concerning the clinical signs of the disease.
The most consistent was scouring and, because this sign preceded
most others in the growing and fatt ening pigs, it is possible that low-
grade pantothenic-acid deficiency could be playing some part in
the general scouring problems that are such a feature of pig
farming today. Many of the weaners and young fattening pigs that
showed a grossly corrugated or necrotic terminal ileitis, and necrotic
colitis at autopsy would, with their clinical history of unthriftiness
and chronic scouring, have been frequently diagnosed as cases of
infective necrotic enteritis or paratyphoid in general farm practice.
PANTOTHENIC-ACID DEFICIENCY IN PIGS
In herd Q, the economic effects of the disease could well have
been limited by the absence of any other major disease burden.
Thus, on a herd basis, the effects of the scouring alone were not as
severe as expected, and many of the pigs that were affected neuro-
logically reached slaughter weight without a gross retardation in
growth. There was, nevertheless, a cumulative and intolerable
economic loss over many months in the fattening pens, excessive
losses among the suckling pigs, and a very serious loss due to inter-
ference with the selection and sale of breeding stock. How the herd
might have fared had it also been affected with enzootic pneumonia
is unknown, but there is some evidence from the feeding trials in
Cambridge to suggest that the 2 conditions together could have been
worse than the combined effects of each alone. Whether the increase
in coughing at the height of the problem in herd 10, however, was
due entirely to an increase in the incidence and effect of enzootic
pneumonia can be questioned; for, in herd Q, coughing was likewise
fairly common in many fattening pens when the deficiency signs
were most wide-spread. There was a slight lung-worm problem in
herd Q at the time, but the extent and degree of the lung-worm
infestation was not of the order that would normally be expected to
produce persistent coughing in litters kept on concrete since weaning
and approaching bacon weight.
CONCLUSIONS
In a herd of Landrace pigs in which the average growth rate was
high, signs of pantothenic-acid deficiency appeared: lack of vigour
in the new-born litters, loss of hair in young growing pigs, scouring,
and varying degrees of neurological involvement. Analysis of the
home-mixed diet showed a deficiency of pantothenic acid.
In controlled experiments on the affected farm, half the pigs in a
number of litters were given a supplement of calcium pantothenate.
All the clinical signs were prevented, provided that the supplement
was given early enough. Although other deficiencies might have
existed at a lower level, pantothenic acid was probably the prime
deficiency. The disease was subsequently eliminated from the herd
by fortifying the diet routinely with a commercial mixture of the
group-B vitamins.
Therapeutic experiments, using dried yeast or calcium panto-
thenate, had no significant effect on the neurological signs, but
brought some improvement in the scouring.
Other herds with a high average rate of growth were then
examined, and a proportion of these showed clinical evidence of
pantothenic-acid deficiency on a smaller scale.
A second form of pantothenic-acid deficiency was seen in herds
in which the rate of growth of the fattening pigs was not unusually
high. In one such herd, a marked vitamin deficiency, as shown by
dietary analysis, was probably due to the excessive use of biscuit-
wafer meal and bread-crust crumbs in the home-mixed meal.
R. F. W. GOODWIN
Neonatal losses were more severe and loss of hair in suckling pigs
more common; the fattening pigs showed scouring and neurological
signs, as in the first herd investigated. The serious effects of the
disease were arrested by fortifying the diet with a multiple mixture
of the group-B vitamins.
The implications of these findings are discussed in relation to the
developing pattern of the British pig industry.
ACKNOWLEDGMENTS
I am pleased to record the kind assistance and interest of several
people and organisations. Mr. A. R. Jennings co-operated in this work
by making pathological observations on a number of the cases that were
brought to Cambridge; his collect,ion of neurological specimens will
probably form the basis of a separate communication. My colleague,
Dr. J. T. Abrams, has been most helpful at all times. Mr. G. H. Clement
of Roche Products Ltd. supplied the calcium pantothenate and arranged
for Hoffmann-La Roche & Co. (Swi tzerland) to place their experience at
my disposal. Mr. S. A. Price of Vitamins Ltd. carried out all the assays for
pantothenic acid. The still photographs were taken by Miss. J. Minns,
who also prepared the prints originating from 16 mm. cine-film. The
latter film was taken by Mr. H. D. Williamson. Most of the expenses were
met by a grant from the Agricultural Research Council.
REFERENCES
Briggs, G. M., and Daft, F. S. (1954). The Vitamins, vol. II, p. 664, ed.
Sebrell, W. H. , and Harris, R. S. Academic Press; New York.
Colby, R. W., Cunha, T.J., Lindley, C. E., Cordy, D. R., and Ensmingel,
M. E. (1948). }. Amer. vet. med. Assoc., 113, 589.
Doyle, L. P. (1937). Ibid., 43,656.
Goodwin, R. F. \V., and Whittlestone, P. (1960). Vet. Rec., 72, 1029.
Hodgskiss, H. W. , Ensminger, M. E., Colby, R. W., and Cunha, T. J.
(1950). J. animo Sci., 9,619.
Hughes, E. H. (1942). ] . agric. Res., 64, 185.
Hughes, E. H., Crampton, E. W., Ellis, N. R., and Loeffel, W . .J. (1944).
Report qf the Committee on Animal Nutrition. II Recommended Nutrient
Allowancesfor Swine. National Research Council; Washington, D.C.
Hughes, E. H., and Ittner, N. R. (1942) .]. animo Sci. , 1,116.
Luecke, R. W., Hoefer,J. A., and Thorp, F. (1952). Ibid., 11, 238.
Luecke, R. W., McMillen, W. N., and Thorp, F. (1950). Ibid. , 9, 78.
Leucke, R. W., Thorp, F., McMillen, W. N., and Dunne, H. VV. (1949).
Ibid., 8, 464.
Leucke, R. W., Thorp, F., Mc11illen, W. N., Dunne, H. W., and
Stafseth, H. J. (1949). Technical Bulletin 21 I. State College Agri-
cultural Experiment Station; Michigan.
McKigney, J . 1., Wallace, H. D., and Cunha, T. J. (1957). ]. animo Sci.,
16,35
Moustgaard, J., and Thorbek, G. (1949). Report XIVth Int. vet. Congress,
London, 3, 63.
Schulze, W. (1960). Dtsch. tieriir::.tl. Wschr., 67, 245.
Ullrey, D. E., Becker, D. E., Terrill, S. W., and Notzold, R. A. (1955) .
]. Nutr., 57,401.
PANTOTHENIC-ACID DEFICIENCY IN PIGS
Wiese, A. C., Lehrer, W. P., Moore, P. R., Pahnish, O. F., and Hartwell,
W. V. (1951). J. animo Sci., 10, 80.
Wintrobe, M. M., Follis, R. H., Alcayaga, R., Paulson, M., and
Humphreys, S. (1943). Johns Hopk. Hosp. Bull., 73, 313.
Wintrobe, M. M., Miller, J. L., and Lisco, H. (1940), Ibid., 67,377.
Wintrobe, M. M., Miller, J. L., Follis, R. H., Stein, H. J., Mushatt, C.,
and Humphreys, S. (1942). J. Nutr., 24, 345.
[Received for publication, December 13th, 1961]
Fig. 1.
Fig. 2.
Fig.
3
Fig.
4
Fig.
5
Fig. 6.
Fig.
7
Fig. S.
Fig.
9
Fig. 10.
Fig. II.
Fig. 12.
R. F. W. GOODWIN
Platf I
Marked goose-stepping, side-view.
l\1arked goose-stepping, rear-view.
Very exaggerated goose-stepping in a running pig, showing lack of flexibility
in the hock joint.
Moderate but obvious goose-stepping in 2 pigs from group B, test I. (Fed the"
unfortified ration. )
Normal gait, for comparison, in 2 control pigs from group A, t est 1. (Fed the
same ration as the pigs in Fig. 4, except for a supplement of calcium panto-
thenate.)
Sudden snatching-movement with a hind leg while standing still.
Similar isolated movement while standing still in another pig, but here there
was a sudden backward, horse-like kick.
Abnormally low position of the hocks.
Deformation of the forelegs, with goose-stepping of the hinds, giving a tip-toe
movement.
The pig on the ri ght could j ust walk, the hind quarters being continuously on
the verge of collapse. The left-ha nd pig required assistance to stand.
Marked swaying of hind qua rters, with splaying of the hind legs.
Sudden collapse on turning q ui ckly. The shock of collapse has thrown the ears
well up.
Note. Figs. I to 12 were prepared from 16 mm. cine-films.
To /ace page 232
PANTOTHENIC-ACID DEFICIENCY IN PIGS
Plate 2
-
Fig. 13. Re-growing hair-stubble on a stunted pig, 6 weeks old, recovering from almost
total baldness. Alopecia was first observed at 4 weeks of age ; thereafter, the
hair could be pulled out easily.
Figs. 14 to 17. Gastritis and intestinal changes in pigs dying in the second feeding
experiment at Cambridge. (These pigs were removed as weaners from the
farm when the disease in herd Q was at its height. Although they suffered from
a febri le condition before death, no other explanation could be found for the
alimentary changes. The febrile nature of the disease is incompatible with
virus transmissible gastro-enteritis, and pooled faeces from 2 cases produced no
ill-effects when fed to a colostrum-depri ved pig that had been reared in isolation.
Gastritis and similar bowel changes were seen in pigs removed straight from
herd Q).