Mycotoxicosis in swine

Dr Kedar Karki
Central veterinary Laboratory
Kathmandu Nepal
 Mycotoxicosis in pigs:
• Mycotoxicosis is a term that refers to the
toxicity that occurs when hogs eat grain
that has a growth of molds. These molds
grow in feed or in the grains used to make
feed if the grain is damp, improperly
stored, or if equipment is not cleaned of
damp grain in between processing. Feeders
that are not water-tight can cause an
overgrowth in warm, damp conditions as
well.
 Effects:

• Inappetence, death,
hyperoestrogenism, infertility, small
litters.
 Mycotoxins
• 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
• 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
• 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
• 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.
 Fumonisin B1
• . 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
• 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).
 fumonisin intake
• 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.
 Ergot
• 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 used.
• Liquid toxinbinders like toxol toxolivum
along with immunolyte immunocare will
be benificial
• 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.