Mypigs

Polish Academy of Sciences, Institute of Genetics and Animal Breeding, Jastrzêbiec, Poland Animal welfare – environment – food quality interactions: Influence some mycotoxins on health and productivity of
Most frequently occurring and particularly dangerous mycotoxins in feeds for pigs are: deoxynivalenol (DON), zearalenone (ZEA) and ochratoxin A (OTA).
Deoxynivalenol (C15H20O6; toxicity: DL50 = 0.75 mg/kg; rats, taken oral y) belongs to
trichotecen group represented by more than 60 different poisons produced mainly by
mildew fungi Fusarium graminearum, Fusarium culmorum and Fusarium nivale.
Typical subclinical symptoms of swine poisoning by deoxynivalenol are loss of
appetite, vomiting and diarrhoea. These indications of the diseases can be
distinguished by breeder after animals consumed fodder with high concentration of
DON. However, in practice such cases occur rarely. Relatively more dangerous for
animals and causing economical losses is consumption of small quantities of
deoxynivalenol during a longer period of feeding.
Besides the visible and recognisable symptoms of animal poisoning, also subclinical state occurs which are characterized by essential changes in morphological composition of blood. In some research (Richter, 1989; Richter et al., 1996) fodder containing 1 mg DON/ 1 kg feed, did not have significant effect on the red blood cells in the fattener pigs. However, changes in white blood cel s were ascertained and manifested by higher number of neutrophil granulocytes and increased number of other forms of granulocytes. Increased concentration of segmented nucleus neutrophil granulocytes in blood of pigs is a typical state explaining DON toxin poisoning. Changes in white blood cel s, in the initial stage of intoxication of the animal’s organism, leads inevitably to neutrophil granulocytosis. Further effect is decrease of lymphocytes contents in animal’s blood. In extreme cases maintaining low level of lymphocytes in blood causes lymphocytopenia (decreased contents of lymphocytes below the reference value) which in turn is responsible for the disruption of the synthesis and function of the bone marrow and blockage of the immune mechanisms in the cell level (immunosuppression). In fattener pigs fed with fodder containing deoxynivalenol an increased activity of asparagine aminotransferase and glutamine aminotransferase was also found, indicating disruptions in metabolism and physiological degradation of cells. Paral el occurrence of significantly increased activity of glutamine dehydrogenasis and gamma glutamine transferase is an evidence of an excessive workload for liver related to biliary ducts disease. Polish Academy of Sciences, Institute of Genetics and Animal Breeding, Jastrzêbiec, Poland Feed containing natural y produced trichotecens used in feeding experiments confirmed big diversity of clinical symptoms of poisoning by deoxynivalenol, indicating that also other mycotoxins participate in the poisoning. It was found that in some cases when the concentration of DON is 1.3 - 3.5 mg in 1kg of given feed ration, significant decrease of feed intake by fatteners was noticed (Young et al., 1983; Bergsjo et al., 1993). In other study (Cote et al., 1984) contents of 2.5 - 4 mg of DON/1 kg feed resulted in decrease of pig reproduction indices, without previous noticeable losses of appetite of animals. In Richter’s study (1989) it could not be demonstrated that loss of appetite causes decrease of body growth when consuming feed contaminated by deoxynivalenol (0.1 mg /1 kg of fatteners body weight) during the whole fattening period. Significant differences in body weight gains of fatteners were not proven between control and experimental groups when the experimental pigs received during fattening period 2.9 mg DON in 1 kg of daily feeding ration (Friend et al., 1986). The quoted authors concluded that there is a decrease of feed intake of daily body weight gains of fatteners when feed is contaminated at the rate of 5.3 mg DON in1 kg feed. Most frequent symptoms of animal poisoning by deoxynivalenol are, besides loss of appetite and decrease of body weight gains, vomiting and diarrhoea. Vomiting occurs seldom and is an outcome of acute poisoning (more than 20 mg of DON/kg in feed) and is resulting usually in animal death. To avoid the above mentioned problems the contents of deoxynivalenol in feed for pigs should not exceed 1 mg/kg. Zearalenone (C18H22O5; toxicity: DL50 >500 mg/kg; mice, into peritoneum) it is also
cal ed F-2 toxin. It is derivative of resorylic acid. Besides type α and β, more than
other 10 chemical forms of zearalenone, are known. Main producers of this toxin are mildew fungi Fusarium, mostly species: F. graminearum, F. culmorum and F. moniliforme. Zearalenone causes disruptions of hormonal regulation of estrogens in swine responsible for reproduction processes. Typical symptoms of toxic effect of zearalenone in sows consuming only 0.05 mg of ZEA in 1 kg of feed are redness, swel ing and inflammation of external sex organs. Long term feeding with fodder containing in 1 kg 0.12 mg of ZEA causes chronic toxic poisoning in pigs. Parallel to the above mention symptoms, which are noticeable to the breeder, other not noticeable symptoms of sow poisoning as chronic il nesses can occur. They can cause uterus enlargement fol owed by forming of cysts on the wal s of the uterine duct (Bauer et al., 1987). It was also found that a high concentration of zearalenone in the feed (3.6 mg/kg) leads to fast progressing impairment of synthesis and distribution of estrogens which causes lack of oestrous and underdevelopment or atrophy of the Corpus luteum. As a consequence of those processes, disorders of the reproduction cycle leading to infertility in sows may occur (Etienne and Jemmali, 1982). When these physiological dysfunctions are occurring in sows’ also significant increase in the rate of aborts was observed as wel as a lower weight of the litters and decreased vitality of the newborn piglets. Zearalenone consumed in feed is partly excreted with sow’s milk (Roth et al., 1990) and can negatively influence health and growth of suckling piglets. More resistant to harmful effect of zearalenone are boars, although some studies show that after receiving higher doses of toxin (40 mg Polish Academy of Sciences, Institute of Genetics and Animal Breeding, Jastrzêbiec, Poland of ZEA/kg of feed) a smaller concentration of spermatozoons in the semen and the testicles atrophy can occur (Stöhr et al., 1990).
Ochratoxin A (C20H18NO6Cl; toxicity: DL50 = 20-22 mg/kg; rats, orally taken) belongs
to 10 groups of ochratoxins produced by various strains of mildew fungi from
species: Aspergil us ochraceus and Penicillium viridicatum. Ochratoxin A is
recognized as a toxin damaging mostly kidney cells and having carcinogenic and
immunosuppressive effects on the organism. Studies carried on pigs (Munro et al.,
1974; Krogh et al., 1974; Plank et al., 1990) confirmed the occurrence of few smal
changes in kidneys when the contents of OTA was 200 µg/kg fodder. Krogh (1987)
found , that in the kidney of pigs fed with fodder containing 200 µg OTA / 1 kg, the
concentration of this toxin did not exceed doses allowed as the norm by the Danish legislation (10 µg/kg tissue). Precautions is very important because the OTA can occur together with other mycotoxins, e.g. citrinin (Szebiotko et al., 1981) which can strengthen the possible poisoning effect. It is acknowledged that safe dose of ochratoxin A (less than 200 µg/kg fodder) does not cause poisoning in pigs, although can cause dysfunction of kidneys. Feeding of young piglets (28-35 days old) with feed containing even low does of OTA (19 µg/kg of feed) causes diarrhoea and death of the animals (Jarczyk et al., 2000).
Literature
1. Bauer J., Heinritzi M., Gareis K., Gedek B.: Veränderungen am Genitaltrakt des weiblichen Schweines nach Verfütterung praxisrelevanter Zearalenonmengen. Tierärztliche Praxis 15, 33-36, 1987.
2. Bergsjo B., Langseth W., Nafstad I., Jansen H., Larsen K.J.S.: The effects of natural y deoxynivalenol-contaminated oats on the clinical condition, blood parameters, performance and carcass composition of growing pigs. Veterinary Research Communications 17, 283-294, 1993.
3. Cote L.M., Reynolds J.D., Vesonder R.F., Buck W.B., Swanson S.P., Coffey R.T., Brown D.C.: Survey of vomitoxin-contaminated feed grains in midwestern United States, and associated health problems in swine. Journal of the American Veterinary Medicine Association 184 (2), 189-192, 1984.
4. Etienne M., Jemmali.: Effects of zearalenone (F2) on estrous activity and reproduction in gilts. Journal of Animal Science 55, 1, 1-9, 1982.
5. Friend D.W., Trenholm H.L., Thompson B.K., Prelusky D.B., Hartin K.E.: Effect of deoxynivalenol (DON)-contaminated diet fed to growing-finishing pigs on their performance at market weight, nitrogenretention and DON excretion. Canadian Journal of Animal Science 66, 1075-1085, 1986.
6. Jarczyk A., Rogiewicz A., M³ynarczyk M., Bancewicz E.: Próba oceny wra¿liwoœci prosi¹t na zawartoœæ w mieszance wysokiego i niskiego Polish Academy of Sciences, Institute of Genetics and Animal Breeding, Jastrzêbiec, Poland stê¿enia ochratoksyny A oraz na obecnoœæ w niej antybiotyku. Biuletyn Naukowy UWM Olsztyn 7, 83-90, 2000.
7. Krogh P.: W: Mycotoxins in Food. Academic Press, London, 1987.
8. Krogh P., Axelsen N.H., Elling F., Gyrid-Hansen N., Hald B., Hyldegaard-Jensen J., Larsen A.E., Madsen A., Mortensen H.P., Moller T., Petersen O.K., Ravnskov U., Restgaard M., Aalund O.: Experimental porcine nephropathy changes of remal function and structure induced by ochratoxin A contaminated feed. Acta Phathologica et Microbiologica Scandinavica 246, 1-21, 1974. 9. Munro I.C., Moodie C.A., Kniper-Goodman T., Scott P.M., Grice H.C.: Toxicological changes in rats fed grades dietary levels of Ochratoxin A Toxicol. Applied Pharmacology 28, 180-188, 1974.
10. Plank G., Bauer J., Grünkemeier A., Fischer S., Gedek B., Barner H.: Untersuchungen zur praktischen Wirkung von Adsorbentien gegenüber Ochratoxin A beim Schwein. Tierärztliche Praxis 18, 483-489, 1990.
11. Richter W.: Untersuchungen zur Entgiftung von zearalenonhaltiger Gerste. Bayerisches Landwirtschaftliches Jahrbuch 66, 2, 219 – 224, 1989.
12. Richter W.I.F., Lepschy J., Gleissenthal V., Lindermayer H., Holzer A., Obst A., Gareis M.: Behandlung von mit Fusarium culmorum infiziertem Winterweizen mit Konservierungsstoffen. Das wirtschaftseigene Futter, 42, 2, 143-160, 1996.
13. Roth L., Frank H., Kormann K.: W: Giftpilze, Pilzgifte. Ecomed, Verlagsgesellschaft mbH Landsberg/Lech, 250-262, 1990.
14. Szebiotko K., Che³kowski J., Dopiera³a B., Godlewska B., Radomyska W.: Mycotoxins in cereal grain. Part 1. Ochratoxin, citrinin, sterigmatoxin, penicillic acid and toxigenic fungi in cereal grain. Die Nahrung 25, 5, 415-421, 1981.
15. Stöhr B., Busch A., Watzke H., Mül er H., Reetz I., Wagner U., Stoyke A., Lepom P:. Der Einfluss von Mykotoxinen auf die Leistung und die Gesundheit von Besamungserben. 12. Mykotoxin Workshop, 21.5-23.5 1990, BLT Grub. Kurzfassungen, 1990.
16. Young J.C., McGirr L., Valli V.E., Lumsen J.H., Lun A.: Vomitoxin in corn fed to young pigs. Journal of Animal Science 57, 3, 655-664, 1983.

Source: http://lhu.emu.ee/downloads/Welfood/WP3T6L4.pdf