Mycotoxicosis in swine

Dr.Kedar karki
Occurrence: Worldwide

Age affected: All ages

Effects: Inappetence, death, hyperoestrogenism, infertility, small

litters.

Mycotoxins are produced by mould growing on crops or stored feeds.

Zearalenone (fusarium F2 toxin) is oestrogenic and is produced with
deoxynivalenol (vomitoxin) by Fusarium spp. growing in wet stored
barley. Aflatoxin is produced from spoiled groundnut or mould finished
feeds by Aspergillus flavus and fumonisin is produced by Fusarium
moniliforme (Giberella fujikourol) growing on maize. Ochratoxin A is
produced by Penicillum viridicatum in mouldy rye and barley and by
fungi such as Aspergillus ochraceous in maize. Ergotamine is produced
by ergot (Claviceps purpurea) growing on rye and wheat and on over-
mature ryegrass. Mycotoxins are ingested in feed to cause their effect.

Zearalenone acts as an oestrogen to disrupt breeding cycles and

reduce the viability of litters, vomitoxin causes vomiting and feed
refusal, aflatoxin causes liver damage such as fatty change, lobular
necrosis, bile duct proliferation and death, and cirrhosis of the liver. At
low levels Fumonisin B1 causes liver damage and higher levels cause
acute pulmonary oedema followed by death. Ochratox A causes
decreased kidney function. Urinary glucose and protein levels of the
urine rise and the concentrating power of the kidney is lost.
Ergotamine in ergot causes constriction of the smaller arteries to cause
abortion and gangrene.

Clinical signs

Zearalenone ingestion by sows in late pregnancy may result in the

birth of small litters, stillborn and weak, splay-legged piglets. Vulval
enlargement may occur in the sow and other female stock on the same
ration. The subsequent breeding behaviour of such females may be
affected ingestion of vomitoxin results in vomiting, feed refusal and
growth depression. Aflatoxin poisoning appears within 6 weeks as
depressed growth rate, inappetence, arched back and apathy.
Jaundice, ataxia and convulsions may occur before death. Fumonisin
toxicity begins with watery diarrhoea followed by a progressive
increase in respiratory rates (to 60-100 per minute). At low levels of
fumonisin intake, there is progressive hepatic disease, but at high
levels mild respiratory distress, pulmonary oedema and death occur.
Ochratoxin A causes reduction in appetite and in the rate of daily live
weight gain and causes polydypsia and polyuria in fattening and adult
pigs. In recently weaned pigs, subcutaneous oedema, ataxia, stiff
arched back and distension of the lumbar part of the abdominal wall
may be seen followed by death in 1 or 2 days. Ergot is an uncommon
cause of agalactia and the birth of small, weak, short-lived or dead
piglets. Extremities such as the ears may become dry or gangrenous.

Diagnosis

Mycotoxicosis may be suspected when mould feed is eaten. Clinical

signs of mycotoxicosis may be recognised. Stillbirths and splay leg
accompanied by vulval enlargement and oedema of mammary tissue
in the presence of stillbirths and splay leg may be cause by
zearalenone. The uterus is heavy and turgid and degenerating
blastocysts may be present form 14-25 days post-service. Aflatoxicosis
may be suspected when growth rate is depressed and inappetence and
jaundice are followed by death. Jaundice of the carcase, a white, tan
or orange liver, oedema of the gall bladder wall, failure of the blood to
clot and microscopical evidence for regeneration of the damaged liver
provide further evidence. Raised pulmonary oedema and liver changes
are obvious at post-mortem examination. Increased thirst and polyuria
may suggest ochratoxicosis and enlarged pale kidneys are present at
post-mortem examination. Agalactia and the birth of small, weak,
short lived or dead piglets in sows at pasture without enlargement of
the teats and udder or which gangrenous extremities suggest ergot
poisoning. Mycotoxicosis is confirmed by laboratory demonstration of
toxin in tissue from affected pigs or in feeds at levels known to cause
disease.

Treatment and control

There is no specific treatment for mycotoxicosis, but affected animals

should be supported (especially piglets born to sows with zearalenone
toxicity) until recovery occurs. Recovery is unlikely in acute
aflatoxicosis and fumonisin poisoning or when the gangrenous form of
ergot poisoning has occurred. In all cases, animals with suspected
mycotoxicosis should be removed from the feed responsible. Control of
mycotoxicosis is achieved by reducing the level of mycotoxin ingested.
Mycotoxin-free feed can be used to dilute contaminated feed down to
the no effect levels. Feed used for dilution must be analysed fro
mycotoxin, but visible mould provides a guide to its presence. Some
proprietary products can reduce the amount of mycotoxin in the feed,
but dilution is most widely used. The use of mould inhibitors should be
considered where mould growth after harvesting leads to mycotoxin
contamination. Calcium propionate, sorbic acid and propioninc acid
may all be sued. Rapid drying of grain may also arrest the
development of moulds. Routine bin hygiene is of major importance in
the prevention of mycotoxicosis. If aflactoxin and ochratoxin are
detected in meat or kidney tissue, carcases exceeding the permitted
level will be destroyed, so animals with mycotoxicosis should not be
sent for slaughter for human consumption.