Probable pantothenic acid deficiency in pigs
A disease syndrome characterised by extensive neonatal losses and
posterior paralysis in feeder pigs was referred to the Ministry of Agriculture as a possible exotic disease. Investigation of the case suggested a diagnosis of pantothenic acid deficiency.
The piggery consisted of approximately I00
sows that were housed in individual cubicles
for farrowing, and other classes of pig
housed in pens with concrete floors. Their
diet consisted of bread, peeled potatoes (uncooked chips), biscuit mix, and cheese to
which small amounts of wheat seed husk,
meat and bone meal, and fish meal were
added. A homemade mineral supplement
and adequate quantities of vitamins A, D and
E were also provided. A very small amount
of mixed fruit and vegetables was given to
dry sows, gilts, farrowed sows and piglets.
Clinical history
From November 1994 to January 1995 and
from June to August 1995, there was a very
high neonatal death rate. In the period from
20 June to 13 July 1995,33 sows farrowed.
About 18% of the piglets were born dead,
and 9 1.5% of the total number born had died
before 7 days of age. Typically piglets were
born full term and clinically normal with
good body weights, although three litters
were up to 4 days premature.
Affected neonates were weak, they shivered
and huddled together before becoming moribund and dying. In spite of antibiotic and
supportive treatment the majority died
within 7 days of birth. In 24 of 33 litters all
the piglets died within 48 hours of birth. The
piglets that survived 48 hours varied in condition from unthrifty to healthy and frequently developed a yellowish scour which
often became very watery. The pregnant
sows and gilts were invariably in excellent
condition and health.
In four litters, piglets had neurological signs
at birth which included; shivering, splayed
legs, dog-sitting, and tremors. A few piglets
exhibited posterior paralysis with the hind
legs being dragged behind the body. Only
one of 46 piglets in these litters was clinically normal and survived to weaning age.
From late June 199.5, a neurological
disease was observed in the 3 to 4-monthold pigs after they had been transferred to
the fattening shed. The ataxic growers were
in a group of 340 pigs being fed to bacon
weight. Six growers died as a result of
progressive paralysis and the prevalence
of ataxia on 14 July 1995 was 19 of 334
(6%). By 26 July 1995, nine more had
died and approximately 44 of 325 (13.5%)
were affected. Pigs purchased at 2 to
3 months of age and pigs less than 3
6 Surveillance 25(4) 1998
months old born on the farm were not affected.
The clinical signs included tenderness in the
feet and hind limbs, an arched back, a reluctance to walk and compete for food, “goose
stepping”, adopting a dog-sitting position,
posterior weakness, hind limbs tucked forward when walking, and lesions caused by
trauma on the posterior hind limbs between
hocks and accessoly digits. The clinical
signs were progressive and death occurred in
4 to 6 weeks. No adult sows or gilts were affected.
Laboratory examinations
Twenty-two neonatal piglets were necropsied including six with neurological signs.
There were few gross lesions but subcutaneous oedema was seen in the limbs of ten neonates, over the body and eyelids in six, and
in the mesentery between the colonic coils in
two. There was severe hydropericardium in
two piglets. Necropsies were performed on
one dead grower and two live growers sacrificed for necropsy. No gross lesions were
detected. A wide range of tissues was taken
from both groups for laboratory examination.
Four piglets and three growers with neurological disease had Wallerian degeneration
of the peripheral nerves (sciatic and brachial
plexus examined), degeneration of the dorsal
roots and degeneration of the dorsal funiculi
in the spinal cord(5).Until this finding there
had been no “link’ between the two apparently different syndromes. In piglets with diarrhoea there was blunting of intestinal villi,
with colonies of bacteria surrounded by neutrophils in the lamina propria at the apex of
the shortened villi. A few of these piglets
also had necrosis of the superficial third of
the colonic mucosa.
No histological lesions were seen in the piglets with gross lesions of subcutaneous oedema. One of the piglets with hydropericardium had locally extensive acute coagulative
necrosis of the left ventricular myocardium.
Samples for serology and virology were examined by the Wallaceville Animal Health
Laboratory and PRRS serology was done at
the Australian Animal Health Laboratory.
Blood samples for serology were collected
in a stratified random manner, three from
each of the following groups; pregnant sows
which had lost litters at their last farrowing,
Roy Sproule, author of this article
pregnant sows which reared their last litter,
pregnant gilts, recently farrowed sows that
lost their litters, normal fatteners, ataxic fatteners, normal weaners, and thin weaners.
Results
The following exotic diseases were excluded
by appropriate combinations of clinical
manifestations, gross pathology, viral culture, serology, and histology - classical
swine fever, Japanese encephalitis B, transmissible gastroenteritis, haemagglutinating
encephalomyelitis and PRRS. Endemic diseases which were excluded in the same way
were Aujeszky’s disease, encephalomyocarditis, viral encephalomyelitis and leptospirosis.
There was no correlation between sires and
dying litters. Previous history of litter loss or
survival was not a factor in subsequent litter
loss. All pigs were fed and watered from the
same source and survivors were apparently
spatially unrelated. These factors helped rule
out inherited or congenital disea:seand toxicosis.
The clinical picture and histological lesions
of the goose-stepping growers were similar
to descriptions of pantothenic acid deficien~y(’)(*)(’)(~).
Goodwin‘’) described a clinical
outbreak of pantothenate deficiency in
which an average of three piglets per litter
were born dead or died soon after birth. The
ration in the outbreak showed a marked similarity to that in the present outbreak. U1lery(*)described an outbreak in which 56%
of pigs born alive in a deficient group died
before 14 days, but did not attribute this necessarily to pantothenic acid deficiency.
When pantothenic acid deficiency was suggested as a probable cause, the owner sup-
plemented the ration of his ataxic weaners
with newly mown grass. Within 48 hours a
noticeable difference in pig vitality was evident. There was no clinical improvement in
the “goose stepping” of affected pigs, but
they were no longer reluctant to stand. The
pigs competed vigorously for food and put
on weight.
An injectable vitamin B preparation”, containing B 1, B2, nicotinamide, B6, D-panthenol, B12 and B15, was administered to a
newly farrowed sow and her piglets on 4
August. The following day, 6 of 13 piglets
were dead, but the rest survived and thrived.
All sows received the multi-vitamin B injection prior to farrowing and newborn piglets
were injected the day they were born. Subsequently one gilt had a litter of dead piglets on
11 August and one sow farrowed a mummified litter on 22 August, but otherwise the
only losses were the few deaths which occur
commonly at farrowing time.
By 10 August a balanced mineral and vitamin supplement had been incorporated into
the ration and thereafter the pigs thrived; the
owners claiming that the pigs were healthier
than they had been for years.
The strength of association between deaths
before and after vitamin B supplementation
showed a relative risk of 3.8, an odds ratio
19.6 and chi-squared was 208.3. The attributable risk was 0.626 (ie more than 62 of
every 100 pigs born died because of vitamin
B deficiency).
Discussion
Many of the clinical signs and histological
lesions, particularly in the grower pigs, were
typical of those described in pantothenic
acid deficiency. Although feed samples were
not tested for their vitamin content, it seems
probable that the diet was deficient in B
group vitamins. The dramatic reduction in
neonatal mortality and the cessation of new
cases of ataxia in growers after the institution of vitamin B therapy supported this diagnosis.
Acknowledgements
Thanks to Drs K R Houston and G L Welten
of Chartwell Veterinary Hospital, Dr Barry
Stevenson of the Monogastric Research
Centre, Massey University, and most of all to
Ted, Irene and Chris, the owners, who have
been cheerful and optimistic even in their
darkest hours.
occurring pantothenic acid deficiency in
pigs. Journal of Comparative Pathology
72, 214-33, 1962
Ullery DE, Becker DE, Terrill SN, Notzold
RA. Dietary levels of pantothenic acid and
reproductive performance of female
swine. Journal of Animal Science 57, 40114,1955
Hodgskiss HW, Ensiminger ME, Colby
RW, Cunha TJ. Inadequacy of purified
diets for reproduction by swine with
observations on an added deficiency of
pantothenic acid. Journal of Animal
Science 9, 619-24, 1950
Blair R , Newsome F. Involvement of
water-soluble vitamins in diseases of
swine. Journal of Animal Science 60(6),
1508-17, 1985
Done JT. The pathological differentiation
of diseases of the central nervous system
of the pig. Veterinary Record 69, 1341-49,
1957
* Multiject B (Bomac Laboratories Limited)
Roy Sproule
Veterinary Officer, Hamilton
MAF Quality Management
References
Rob Fuirley
MAF Quality Management
Ruakura Animal Health Laboratory
(1) Goodwin RFW. Some clinical and
experimental observations on naturally-
Accepted for publication September 1997
Surveillance 25(4) 1998
7