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This article was published in 1983
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Vitamin A Deficiency in Pigs

J.V. Evers, B.V.Sc., Veterinary Inspector, YOUNG

Vitamin A deficiency has often been diagnosed in grazing stock under drought conditions. It is also reported from time to time in intensive-rearing systems. This paper describes a neurological syndrome seen in two semi-intensive piggeries in the Young District during drought conditions in 1982 - Vitamin A levels and histopathology indicated that the syndrome was a manifestation of Hypovitaminosis A.

CASE 1

An 8 sow unit; sows run out on bare granite hilltop; weaners placed in grower pens at 6-8 weeks; home-mix ration with wheat/10% meatmeal/growth promotant and continuous Hygromycin treatment - no mineral/vitamin additive.

20/8/82 - investigated stillbirth problem seen in 4 successive litters. Field and laboratory examination indicated a diagnosis of slow parturition and terminal hypoxia. No gross or microscopic defects were noted.

2/9/82 - follow-up visit revealed an ataxia problem in 10 ex 40 growers of perhaps 6 months duration and paresis was noted in a freshly-farrowed litter. Histopathology was indicative of Vitamin A deficiency and treatment commenced on 9/10/82.

12/10/82 - plasma and liver samples were collected from treated and control animals and yielded the following results:

Treated:- Plasma - 1.28 (Normal:- 0.7-0.9 u mol/L).

Controls:- Plasma - 0 to 0.20.

Treated:- Liver - 472.0. (Normal:- 25-116 u mol/kg).

Control:- Liver - 2.7.

25/10/82 - a good response to treatment of affected growers with 500,000 - 1,000,000 I.U. Vitamin A ('JANAJEC' 1-2ml.) was noted, with full recovery by 9/11/82.

Use of a commercial mineral/vitamin premix has been accompanied by a return to normal litter sizes and no recurrence of the neurological syndrome in growers.

CASE 2

An 8 sow unit; sows run out on flat red loam country; weaners moved into grower pens at 10-12 weeks; home-mix ration with barley/15% meatmeal/mineral-vitamin premix and continuous Hygromycin treatment.

15/8/82 - noticed inappetence in 5 ex 20 growers at 20-24 weeks, followed by mild ataxia several weeks later.

29/9/82 - had 3 ex 10 baconers go down during transport to Young Pig Sale - 2 showed hindlimb paresis; 1 showed paralysis, jaw champing, hyperaesthesia and muscle tremors and was euthanased for autopsy. Farrowings in the breeding herd had been normal.

8/11/82 - equivocal findings on histopathology obtained. A slow recovery was occurring in the 2 advanced clinical cases on access to green feed. Treatment with 2cc. 'JANAJEC' was recommended.

1/12/82 liver levels of < 3 (Normal 25-116 umol/kg.) and a revised histopathology report confirmed Hypovitaminosis A. All growers had responded to treatment but the 2 advanced clinical cases still showed mild ataxia and a reluctance to move.

Although used at recommended rates, the mineral/vitamin additive had been purchased about 6 months previously and stored under adverse conditions in a tin shed.

A brief review of some standard texts has provided the following relevant information:-

1. VITAMIN A - chemical and biological properties

Vitamin A or Retinol has the chemical formulation of C20H29OH. It can be provided in animal feeds as the synthetic compound or be synthesised from provitamin precursors - Carotenoids - in the intestinal wall. Green feeds are good sources of Carotenes and may provide up to 100 x normal daily requirements while concentrates - including most grains - are grossly deficient. Retinol is stored in the Liver, and to a lesser extent the kidneys and fat depots. There is poor placental transfer of Retinol but this is normally compensated for by high levels in the Colostrum.

Many factors can affect the availability, synthesis, absorption and storage of Vitamin A:-

2. VITAMIN A - biological functions

Because Vitamins are defined more by deficiency symptoms than by specific biochemical functions, the precise function of Vitamin A is not yet determined.

It appears to be involved in 'hydrogenation metabolism' and this role is manifested more specifically in the following areas:-

Little wonder that a great variety of disorders can be conveniently attributed to a deficiency of Vitamin A!

3. VITAMIN A - symptoms of deficiency

Symptoms of deficiency will vary according to animal species, age, reproductive status, and severity of the deficiency. Growing animals may require levels of around 3x maintenance, while young breeding stock may require up to 5x maintenance.

In mature ruminants liver stores may provide 12-18 months maintenance; in pigs, deficiency symptoms will normally appear within 4-5 months. Symptoms seen in pigs may include:-

Despite the emphasis which many authors place on Vitamin A - related infertility it is likely that other symptoms will precede this syndrome in the individual case. Night blindness - if detectable - occurs earlier, and the neurological syndrome appears to have been in evidence before fertility problems were noted in these 2 herds. Oedema and malformations were not seen in the stillbirths investigated.

The diagnosis of Vitamin A deficiency should not be made without confirmation of depressed plasma or liver levels, but compatible clinical signs + supportive histopathology + a significant treatment response within 2-4 weeks should be considered adequate if Retinol assay is not available. In addition, falsely depressed levels will be obtained if samples are not fresh at collection, protected from light and chilled immediately.

A NOTE ON TREATMENT

Vitamin A can be toxic in overdose, and this may be manifested as:-

Dose rates of 250,000 I.U. in suckers up to 1,500,000 I.U. in heavy pigs would seem to be adequate for short-term therapy if feed levels are concurrently corrected to 3-9 million I.U./tonne.

SOME FIELD OBSERVATIONS

Although I have often seen growing pigs fed on Vitamin A deficient rations before, I have not seen clinical signs of deficiency.

In fact, if sow levels are initially normal the growers will probably finish and be slaughtered before neurological signs become apparent.

Perhaps this is why the stillbirth problem is ultimately the first gross sign of Vitamin A deficiency seen in many piggeries - as sow levels decline over successive farrowings. The provision of different rations to growers and breeders would also complicate clinical manifestations. In this particular case, it is feasible that the sows may have been obtaining small amounts of Carotene from grazing in outside runs. When this was unavailable during drought conditions, the gross Vitamin A deficiency in the ration finally became apparent.

It is also interesting to speculate that regimes of continuous Hygromycin therapy may have potentiated the development of neurological lesions in these two outbreaks.

Finally, the storage of Vitamin Mineral premixes and concentrates should always be a cause for concern. Antagonisms and incompatibilities will be further aggravated by exposure of these mixtures to excessive heat or light and Vitamin A is likely to be one of the first casualties.

References

Animal Health in Australia - Cambell. Vol. 3. 1983

Animal Nutrition - McDonald. 1969

Diseases of Swine - Dunne. 1965

Duke's Physiology of Domestic Animals - Swenson. 1970

Pathology of Domestic Animals - Jubb and Kennedy. 1970

Pig Diseases - Taylor. 1979

Progress in Swine Practice - Vol. 2. 1972

Refresher Course on Pig Diseases - Proceedings 20, 1973; Proceedings 56, 1981

Veterinary Medicine - Blood and Henderson. 1975.

Acknowledgements

V.O. Geoff Marshall (wagga) for assistance with collection of plasma and liver levels

V.R.O. John Glastonbury (wagga) for his advice and interest.

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