Mycotoxicosis in swine

Dr Kedar Karki Central veterinary Laboratory Kathmandu Nepal

• 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.

Mycotoxicosis in pigs:


• 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.

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.

• 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.

Clinical signs

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.

• 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.

• 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.