Mycotoxins in Swine Feed

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Basic Considerations

Fusarium in Wheat and Barley

Wheat, corn, and barley together account for about 65% of the world production of
cereals, and all are susceptible to pre-harvest infection by Fusarium fungi. In addition to
reducing quality and yield, Fusarium also produces mycotoxins that contaminate the
cereal crop. Two of the most important species in this regard are Fusarium graminearum
and Fusarium culmorum. These species typically develop during wet midsummer
weather to produce Fusarium head blight in barley and wheat. These fungi also produce
deoxynivalenol (DON) and related mycotoxins at high enough levels to produce toxic
effects in livestock, especially swine. Disease outbreaks affecting only a fraction of the
heads in a field are capable of producing a crop that exceeds accepted tolerances for
mycotoxins in animal feed.

The mycotoxin usually produced during Fusarium head blight is deoxynivalenol (DON),
although related toxins similar to DON may also be present. Fusarium graminearum can
produce both 3-acetylDON and 15-acetylDON in addition to DON in field crops. This
poses a problem for swine producers because not only is DON present, but these analogs
accompanying DON possess a higher oral toxicity than DON itself. Both DON and 15-
acetylDON have been recently found in wheat and barley from Manitoba and from North
Dakota.

DON is the most widespread Fusarium toxin in Canada, and was discovered in Ontario
and Quebec wheat back in 1980. In western Canada, the first report of widespread
contamination of wheat by DON was in 1985 crops, and other more toxic Fusarium
products such as HT-2 toxin have appeared in subsequent crop years. In 1985-87, and
during the 1990's, Fusarium head blight recurred in Manitoba wheat, and grain producers
became familiar with the sight of shriveled pink or white "tombstone" kernels in
harvested grain.

In the last ten years, southern Manitoba has experienced exceptionally high summer
rainfall, followed by epidemics of Fusarium head blight in barley and wheat. This has
resulted in many deliveries to country elevators of grain having visible Fusarium mold,
and in numerous requests for DON testing in affected crops.

Today, the presence of toxin-producing Fusarium fungi in western Canadian wheat is of
unprecedented concern, owing to the spread of Fusarium graminearum and DON
westward from Manitoba into Saskatchewan and Alberta (Clear et al. 2000), and because
of crop contamination by more toxic products such as HT-2 toxin and moniliformin.


Demise of Grain Transportation Subsidies
In 1995, railway grain transportation subsidies, administered through the Western Grain
Transportation Act of 1984, were terminated by the federal government. The cost of
shipping grain increased sharply from the former Crow's-Nest Pass Agreement (1897)
rates, and it quickly became much more expensive to ship grain from Manitoba to year-round
export ports. With low grain prices, questions have arisen about the future
profitability of grain farming in Manitoba. There has been a large increase in livestock
production, which benefits from low grain prices, and which is not so sensitive to
transportation costs. The most rapid growth has been in the swine production sector, but
this depends on a steady supply of low-cost, wholesome, locally produced feed.


Grain Carryover and Storage Mycotoxins
During 1988-98, the average production of barley in Canada was 12.5 million T. Of that,
approx. 54% was used for feed, and 17% was put into storage. Comparable production
for corn was 6.7 million T, with 68% going to feed, and 11% in storage. During this
period, 26.4 million T of wheat was grown annually on average, and 11% was used for
feed, while 24% was stored (Canada Grains Council 1998).

The carryover of these crops arises from marketing and transportation arrangements, but
creates potential hazards for livestock producers. A one-year storage interval creates
ample opportunity for fungal growth and mycotoxin formation if the moisture content
rises above 15%. As on-farm storage increases over time, chances for spoilage multiply:
moisture condensation in the structure, rain seepage, humid zones from insect infestation,
and convective moisture migration are some of the main causes (Abramson 1997).

In Canada, blue-green Penicillium molds are common in stored foods, feeds, and grains.
These molds are capable of producing ochratoxin A (or more simply, "ochratoxin") at
levels up to 10 parts-per-million (ppm). Such levels are rarely encountered, but
ochratoxin is hazardous to swine at much lower levels, typically 0.2 ppm (Krogh 1991).
If ingested over a long enough period of time by swine, this toxin can contaminate most
of the edible tissues, and can produce enough kidney damage to result in condemning the
carcass. But ochratoxin residues in animal products are transmissible to consumers, and
some national governments have taken stringent measures to allay consumer fears
regarding their pork products. In Denmark, for example, an entire swine carcass is
considered contaminated, and is condemned, if 25 µg/mL ochratoxin is detected in the
blood.


Public Apprehension about Food Contamination
The Canadian system for food safety is one of the most comprehensive in the world, but
most consumers have a limited understanding of the food production system and how
food is regulated and protected (Murphy 1999). Recurring agriculture-related problems
such as bovine spongiform encephalopathy (BSE, mad-cow disease) and beef
contamination in Britain, Escherichia coli 0157:H7 contamination in the USA, and the
fatal contamination of drinking water in Walkerton Ontario, undermine public confidence
in both government and industry. Several television and newspaper corporations have
seen these events as opportunities to exploit consumers' fears and to maximize short-term
profits through increased viewership and readership. Furthermore, television news
accounts of food poisoning in the USA are often wrongly perceived by Canadian viewers
as pertaining to the Canadian food safety situation. The portrayal of American problems
as Canadian problems has been a common practice in the non-technical sector of
Canadian media for decades.

These factors may soon pose problems for producers and food inspection agencies.
Consumers, confused by the many factors involved in food contamination, mistrustful of
government information, and impatient with lengthy multi-year studies of contamination
patterns, may exert political pressure through their associations for simplistic "zero-tolerance"
food legislation solutions.


Fusarium Mycotoxins and their Detection
Of the many metabolites Fusarium fungi can produce, only about a dozen show toxicity
by the oral route of ingestion, and occur as natural contaminants of crops. This group
includes deoxynivalenol (DON), 3-acetylDON, 15-acetylDON, nivalenol, fusarenone,
diacetoxyscirpenol, T-2 toxin, HT-2 toxin, moniliformin and fumonisin B 1 . The fungal
estrogen zearalenone is usually included in this group.

In western Canada, only five of these Fusarium toxins are found in crops. The most
widespread is DON, with highest levels found in barley, and lower levels in wheat. The
contamination of oats by DON is minimal. Other toxins -- 15-acetylDON, T-2 toxin, HT-2
toxin, and moniliformin -- are infrequently encountered in barley and wheat, and
usually at levels far below 0.5 ppm. This is fortunate, since they are 1.5- to 10-fold more
toxic than in DON (Table 1). Toxicity is given as LD 50 , a figure indicating the estimated
lethal dose for 50% of test animals 7 days after oral administration, in mg toxin per kg
body weight. The lower the LD 50 , the more poisonous is the toxin.

In eastern Canada, DON is a common contaminant of feed corn and soft wheat. In
Ontario corn, zearalenone is often present at levels high enough (> 0.5 ppm) to give
estrogenic responses in swine. Fumonisin B 1 has been also reported in some isolated
samples of Ontario corn but at levels generally below 5 ppm, the suggested limit for
feeding to horses. Zearalenone and fumonisin B 1 are more common in American corn,
In eastern Canada, DON is a common contaminant of feed corn and soft wheat. In
Ontario corn, zearalenone is often present at levels high enough (> 0.5 ppm) to give
estrogenic responses in swine. Fumonisin B 1 has been also reported in some isolated
samples of Ontario corn but at levels generally below 5 ppm, the suggested limit for
feeding to horses. Zearalenone and fumonisin B 1 are more common in American corn,
and occur at higher levels.

Commercial enzyme immunoassay kits are available to screen commodities for DON, T-2
toxin, fumonisin B 1 and zearalenone. Contract laboratories can perform the tests within
a few days, at reasonable cost. The most critical part of any analytical procedure for
mycotoxins is sampling the commodity in a truly representative manner (Whitaker 2000).
For example, published studies of aflatoxins in peanuts have shown that only 6% of the
total testing error is due to the analytical method, while 94% is due to sampling and
subsampling problems. Producers and handlers of grain are strongly advised to employ
well-validated protocols in getting representative samples of grain for mycotoxin testing.
This would ensure that end-use decisions regarding the commodity tested are based on
valid results.


Locally, testing is performed on a fee-service basis at:
Canadian Grain Commission
846-303 Main Street
Winnipeg R3C 3G8
(204) 983-3359

(DON, $53)


NorWest Laboratories
545 University Crescent
Winnipeg R3T 5S6
(204) 982-8630

(DON, $29)


Ochratoxin in the Food Chain
Ochratoxin A (or more simply, "ochratoxin") is a potent kidney toxin and causes birth
defects in test animals such as rats, hamsters and mice. The oral LD 50 for ochratoxin in
rats is 22 mg/kg, in day-old chicks, 3.6 mg/kg, and in swine, approx. 6 mg/kg. The
carcinogenicity of ochratoxin in mice has been documented. A study at the National
Institutes of Health in the USA also showed ochratoxin to be a carcinogen in rats.

In terms of animal and human health, ochratoxin is the most important of the Penicillium
mycotoxins. It is particular serious for the poultry and swine industries because
monogastric animals lack the ability to degrade ochratoxin rapidly, as compared to
ruminants. Monogastric livestock are far more susceptible to the nephrotoxic effects of
ochratoxin than ruminants, and toxin residues can enter the human food chain through
organ and meat products. In ruminant livestock, adverse effects are limited mainly to
decreased milk production, and this effect is reversible and transient.

Ochratoxin contaminates a variety of plant and animal products, and is particularly likely
to appear in stored cereal grains. This mycotoxin is a worldwide problem, and its impact
is greatest in temperate climates where much of the world's grain is produced and stored.
In most countries with the technology to survey of cereal-based foods and feeds,
ochratoxin has been found as a contaminant. Cheese is also a good substrate for
ochratoxin production, and this toxin has been discovered in moldy cheese from Britain.
Ochratoxin is found in meat products from monogastric animals, and has been frequently
detected in pork products from Europe. In chickens, this toxin can be carried over from
contaminated feed into muscle tissue and eggs.

Ochratoxin has become a major concern to livestock producers, especially in Europe and
North America. Ochratoxin introduced into the feed of monogastric livestock
contaminates eggs, organs, fat, muscle tissue, and blood. Although limited data is
available for poultry, swine are quite susceptible to contamination owing to a rather long
serum half-life of 72-120 hr. Recent surveys have detected ochratoxins a natural
contaminant of swine blood in Canada (Figure 1), and in many European countries,
including Germany, Norway, Poland, Sweden, and Yugoslavia. In addition, ochratoxin
has been found in swine kidneys in the USA, Austria, Belgium, Denmark, Finland,
Germany, Poland, Switzerland, Britain, and Yugoslavia.

Ochratoxin has also been found in the blood of humans, and has been associated with a
high incidence of kidney disease in parts of eastern Europe. This disease is encountered
in Bulgaria and Yugoslavia, and is known as Balkan endemic nephropathy. Ochratoxin
residues have been compared in food and blood samples from nephropathic and non-nephropathic
regions of this geographical area. Ochratoxin has also been found in human
blood samples from other parts of Europe, including Germany, Poland, and the Czech
Republic. This mycotoxin has recently been detected in human blood in Canada (Scott et
al. 1998), Japan, and Italy.

Canadian surveys for ochratoxin in the blood of slaughter hogs, and in human blood,
have been published, and are summarized in Figures 1 and 2. In swine, the principal
source of ochratoxin is contaminated cereal-based feed. The main sources of ochratoxin
in the human diet are undoubtedly cereal products and pork products, although other
commodities (coffee, wine, beer, cheese, poultry products) may contain traces of this
toxin. These results have occasioned discussion about "safe" levels and the need for
future legislation. In the meantime, however, it is prudent to minimize ochratoxin
residues in pork products, considering consumer apprehension about food safety. In
Europe in 1997 maximum tolerances of 5 parts-per-billion (ppb) for ochratoxin were set
for all foods, and Germany is presently enforcing its own 3 ppb limit.


Fumonisins and Aflatoxins in Imported Corn
During the 1990's, investigations of swine poisoning in the USA identified fumonisins
(B 1 and B 2 ) in feed corn as causative agents of porcine pulmonary edema. Later tests
involving intubation with pure fumonisins, or feeding very highly contaminated feed (200
ppm), showed pulmonary edema, accompanied by liver damage and pancreatic lesions.
Fumonisins commonly contaminate the USA corn crop, and levels of >5 ppm are not
unusual. Screenings and broken kernels contain higher levels.

Aflatoxins are also common contaminants of corn grown in the USA. Highest levels have
been seen in corn from the Southeast in certain crop years. For example, in 1977, 35% of
Georgia corn and 67% of Florida corn had aflatoxins >100 ppb. Corn from midwest
states is generally much lower.

Aflatoxins cause liver damage in swine. USA guidelines establish a maximum of 300 ppb
for total aflatoxins (B 1 +B 2 +G 1 +G 2 ) in swine feed, but specify limits of 200 ppb for
finishing swine, 100 ppb for breeding swine, and 20 ppb for immature animals. European
Community guidelines specify an upper limit of 20 ppb aflatoxin B 1 in swine feed (Smith
1997).


Detoxification of Feed Ingredients
The removal or deactivation of mycotoxins in agricultural commodities has been studied
for almost 30 years. Broadly speaking, the aim of detoxification is to inactivate or remove
the mycotoxin, while leaving no chemical residues from the process. Furthermore, the
palatability and nutritional value of the commodity should be maintained. The low
market price of feed ingredients such as cereal grains requires that detoxification be cost-effective.

So far the only successful chemical deactivation process has been ammonia treatment of
aflatoxin-contaminated corn (Smith 1997). Other chemical treatments are either too
expensive, or degrade the finished product to unacceptable levels. The same appears to be
true for physical methods such as sieving or heat treatment.

Inactivation through binding agents is also economically feasible for aflatoxins. Because
of their unique chemical structure, aflatoxins can be strongly adsorbed or bound by
certain types of clay, specifically hydrated sodium calcium alumino-silicates (HSCAS).
These cheap and effective additives have been used to treat aflatoxin-contaminated
chicken feeds in the USA. Outside of this single application, the worth of binding agents
has yet to be proven in any published scientific study. For example, HSCAS-type binding
additives do not work in the cases where the feeds are contaminated with ochratoxin or
DON (Trenholm et al. 1989).


Summary
1. DON arises from Fusarium in feed grains, and is the main problem for swine
producers. Testing is locally available. Representative sampling is important, especially if
blending is used to reduce DON content.

2. Ochratoxin arises from storage molds in feed grains, and is able to contaminate pork
products at the ppb level. The European Community has restricted the limits of
ochratoxin in food to 5 ppb. While discussion continues about the significance of this
carcinogen in human health, it would be prudent to minimize exposure of swine to moldy
grain, especially at the finishing stage.

3. The decision to use corn in swine feed should be considered only if the levels of
fumonisin B 1 , zearalenone, and aflatoxins are known from actual lot analysis.

4. Although decontamination has worked for aflatoxins through ammonia treatment, or
through alumino-silicate feed additives for poultry feed, no other technologies have yet
been shown to be cost-effective for other mycotoxins in feeds. Claims for additives which
bind DON, other Fusarium toxins, or ochratoxin, have not been validated. Validation
consists of control studies appearing in peer-reviewed scientific publications.
Miscellaneous "reports", or commercial promotion, do not constitute validation.


References
Abramson, D. Toxicants of the Genus Penicillium. Pages 303-317 in: D'Mello, J. P. F.
(ed) Handbook of Plant and Fungal Toxicants (New York: CRC Press, 1997).

Canada Grains Council, Canadian Grains Industry Statistical Handbook 98,
(Winnipeg: Canada Grains Council, 1998).

Clear, R. M., Patrick, S. K., Gaba, D. 2000. Prevalence of fungi and fusariotoxins on
barley seed from western Canada, 1995 to 1997. Can. J. Plant Pathol. 22: 44-50.

Krogh, P. Porcine nephropathy associated with ochratoxin A. Pages 627-645 in: Smith,
J. E., Henderson R. S. (eds) Mycotoxins and Animal Foods (New York: CRC Press,
1991).

Kuiper-Goodman, T., Ominski, K., Marquardt, R. R., Malcolm, S., McMullen, E.,
Lombaert, G. A., Morton, T. Estimating human exposure to ochratoxin A in Canada.
Pages 167-174 in: Creppy, E. E., Castegnaro, M., Dirheimer, G. (eds) Human
Ochratoxicosis and its Pathologies (Paris: Editions INSERM, 1993).

Murphy, L. A. 1999. A Consumer Perspective on Food Safety. Proc. Canadian
Workshop Fusarium Head Blight 28-30.

Scott, P. M., Kanhere, S. R., Lau, B. P.-Y., Lewis, D. A., Hayward, S., Ryan, J. J.,
Kuiper-Goodman, T. 1998. Survey of Canadian human blood plasma for ochratoxin A.
Food Addit. Contam. 15:555-562.

Smith, J. E. Aflatoxins. Pages 269-285 in: D'Mello, J. P. F. (ed) Handbook of Plant and
Fungal Toxicants (New York: CRC Press, 1997).

Trenholm, H. L., Thompson, B. K., Friend, D. W. 1989. Evaluation of hydrated
sodium calcium aluminosilicate in vomitoxin-contaminated diets fed to gilts. Proc. Amer.
Assoc. Swine Practitioners 103-114.

Whitaker, T. B. Sampling Techniques. Pages 11-24 in: Trucksess, M. E., Pohland, A. E.
(eds) Mycotoxin Protocols (Totowa NJ: Humana Press, 2000).


Table 1 Oral Toxicity of Some Toxins and Estrogens Isolated from Fusarium fungi.

Test animal
LD 50 , mg/kg
Type-A trichothecenes:    
T-2 toxin
rat
5.2
chick
5.0
HT-2 toxin
chick
7.2
diacetoxyscirpenol
rat
7.3
chick
3.8
Type-B trichothecenes:
deoxynivalenol (DON)
mouse
46.0
3-acetylDON
mouse
34.0
15-acetylDON
mouse
34.0
nivalenol
rat
19.5
fusarenone
mouse
4.5
chick
33.8
Non-trichothecenes:
moniliformin
cockerel a
4.0
fumonisin B 1
horse
b
Estrogens:
zearalenone
mouse
>5,000

a = one day old
b = leukoencephalomalacia arising from 1-4 mg/kg fumonisin B 1





 
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