Age affected: All ages.
Causes: Bacteria – Streptococcus suis, Haemophilus parasuis, Salmonella etc.; viral. infections; poor ventilation; overcrowding; stress.
Effects: Inappetence, trembling, twitching, abnormal eye movements, convulsions, death.
Mycotoxins are produced by moulds 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 mouldy 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. Ochratoxin 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.
Mycotoxicosis is not transmissible, but can occur in successive groups of pigs receiving the same rations.
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 finishing 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 caused by zearalenone. The uterus is heavy and turgid and degenerating blastocysts may be present from 14-25 days post-service. Aflatoxicosis may be suspected when growth rate is depressed and inappetence and jaundice are followed by death. Increased thirst and polyuria may suggest ochratoxicosis. Agalactia and the birth of small, weak, short lived or dead piglets in sows at pasture without enlargement of the teats and udder or with gangrenous extremities suggests ergot poisoning. Mycotoxicosis is confirmed by laboratory demonstration of toxin in tissue from affected pigs or in feeds at levels known to cause disease.
In sows with zearelenone toxicity, the enlarged mammary glands may be obvious along with enlargement of the vulva. The uterus is heavy and turgid and degenerating blastocysts may be present from 14-25 days post-service. Piglets which have died with splay leg have erosion of the tail root, together with erosion of the swollen vulva in female piglets. In aflatoxicosis there is 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. Pulmonary oedema and liver changes are obvious at post-mortem examination in cases of fumonisin toxicity. In ochratoxicosis there may be enlargement and pallor of the kidneys. Gangrenous extremities may be present in ergotism.
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 for mycotoxin, but visible mould provides a guide to its presence, and the process can only be legally carried out under state veterinary control in the case of aspergillosis. 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. Rapid drying of grain may also arrest the development of moulds. Routine bin hygiene is of major importance in the prevention of mycotoxicosis. If aflatoxin 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.