Clinical signs of mycotoxicosis in pigs and other farm animals represent only the tip of the iceberg regarding health and performance effects due to mycotoxins, warned Professor Johanna Fink-Gremmels from the veterinary faculty at Utrecht University, Netherlands.
Veterinary problems in a 250-sow Norwegian herd have demonstrated the destructive power of toxins from mouldy grains in feeds. In this case the answer took the form of a dietary treatment. Other possible solutions for pig units to deal with feed contamination issues were outlined recently to an international gathering of scientists specialised in mycotoxin control.
For a variety of reasons, the meeting heard, moulds and their toxic products are affecting an increasing quantity of feed grains worldwide. An assessment 2 years ago that mycotoxins could be found in at least 25% of all grains harvested seems now to be an under-estimate. Climate is thought to be one of the factors responsible, along with changes in farming practices and the growing of susceptible crops.
Pig producers in particular should be wary of a possible contamination in the feed they use. Speakers at the 3rd World Mycotoxin Forum, which took place at the end of last year in the Netherlands, were agreed that pigs are the most sensitive of the farm animal species in this respect. Five out of the 300 or more known types of mould toxin are regarded as most relevant to agriculture; the pig is rated first on sensitivity for each of them.
That view has been reinforced by scientific advice given to the European Union's administrators by independent food safety agency EFSA, the forum was told. Referring to major toxins from the globally important fungal genus called Fusarium, it advised that pigs were significantly more sensitive than poultry or cattle to the effects of deoxynivalenol (usually abbreviated as DON) and zearalenone (ZON). Much the same was true for other Fusarium toxins known as fumonisins, for ochratoxin A (OTA) from an Aspergillus fungus and for alkaloids from ergot.
Clinical signs of illness are observed whenever any of these exceeds a threshold level in the pig's diet. For example, the vomiting caused by DON has given it the common name of vomitoxin, but pigs will start to refuse feed and show retarded growth once its presence goes above 5-10 parts per million. ZON was described to the forum as the classic textbook model of how oestrogen receptors work. It has oestrogenic (hormonal) effects on puberty and fertility when present at more than 1-3ppm. OTA can give rise to kidney damage with a dietary level of just 200 parts per billion. Typically a European problem from contaminated wheat or barley, at higher concentrations this ochratoxin is blamed for a so-called porcine nephropathy in which the kidneys become shrunken and discoloured as well as losing their function.
One difficulty with any discussion of clinical signs and threshold levels, however, is that both sensitivity and effect are influenced by the age or production stage of the pig. Nursery pigs will be far more sensitive than a gestating or lactating sow for the impact of a Fusarium mycotoxin on their appetite, possibly because the sows have an instinctive drive to keep eating in order to fuel the development of their unborn piglets or their milk production after farrowing. Effects can also be delayed, such as the subsequent stillbirths from sows consuming mouldy feed in pregnancy or the disrupted endocrine balance in gilts around puberty due to their consumption of zearalenone at an earlier stage.
Then there is the unavoidable fact, again reiterated at the Dutch conference, that moulds rarely if ever occur alone. The pig will therefore be challenged by a combination of mycotoxins acting together and perhaps in a synergistic relationship to create much greater health problems than they would have caused individually. This needs to be remembered when choosing a response, since some forms of feed treatment are effective against only a narrow range of target toxins.
Above all, the forum was alerted to twin dangers in any assessment of the mycotoxin problem in pigs. One is the growing certainty that the observable, clinical signs are only a small part of the overall story. Sub-clinical or non-diagnosed anchors on feed intake, growth and reproduction add up to a considerably higher cost. Secondly, a new concern among veterinarians is the thought that the mould toxins might do the most damage to herd performance by suppressing or impairing the immunity of the pigs that eat the feed.
New data on immunosuppression by mycotoxins will be published shortly, speakers indicated. An impairment of immune competence is being attributed to contaminations with deoxynivalenol, for example, involving both the development of innate immunity and the animal's ability to generate a gut-associated local immune response. There are also lingering suspicions of a mould link to the severity of the wasting disease PMWS and a belief that interactions of some low-level fungal toxins might explain a number of the persistent health problems on many pig units today.
Mycotoxins from mould on the maize plant before harvest can be at increased concentrations in corn by-products.
Levels of the DON and ZON found in maize, wheat, barley and oats vary year by year with climate, season and geography, from a few parts per billion to several hundred milligrams per kilogram. German data presented to the World Mycotoxin Forum showed that there is also a variation with these toxins in complete pig diets. Although only a few samples exceeded the critical concentration for causing disease in piglets, the near-constant background of a baseline level of contamination was revealed by the official test results for a period of several years.
What happens when the toxins combine was illustrated at the meeting by a description of the herd in Norway that found its sows were refusing to eat a purchased feed. This mixture bought from a commercial feedmill had the typically Norwegian grain blend of wheat, barley and oats. Later examination would show vomitoxin (DON) in a local oat variety used by the mill.
While the uneaten feed was returned to the supplier, some had been consumed by the sows and they began to require veterinary attention. Eventually half of the 250 sows in the herd needed treatment at or around farrowing time, mainly for a condition resembling mastitis-metritis-agalactia or MMA. Total antibiotic usage escalated to 25% above its usual rate. An antibiotic therapy employed to combat E. coli failed to work, even though it had checked out as correct in laboratory tests.
The veterinary clinic advising the herd concluded that the mycotoxin discovered in the breeder feed had both direct and indirect effects. It affected the immunity of the sows themselves and of their progeny, besides upsetting the effectiveness of therapeutics. The problem was remedied by top-dressing a replacement feed with a proprietary product that detoxified certain toxins through microbial degradation and bound others onto an adsorbent material.
Clays that have been specially chosen to bind toxin elements comprise one of the most traditional strategies against moulds in feeds, said forum attendees. The product information on binders is most complete with regard to their use in controlling aflatoxins, against which virtually all products on the market are effective. Even so the information confirms generally that not all clays are the same in the sense of having the correct structure to immobilise these toxins; international studies were said to have identified so-called hydrated sodium calcium aluminosilicate or HSCA materials as performing consistently well versus aflatoxins, while being less reliable at dealing with DON and ZON. What is more, under some circumstances there could be the risk that the adsorbent also binds nutrients.
More mould inhibitors on the market contain yeast cell wall materials that have an affinity for a larger range of mycotoxins. The list of possibilities has been extended again recently by the discovery of a novel yeast with the ability to devour and inactivate ochratoxin A and zearalenone.
Piglets represent the biggest challenge in relation to a mycotoxin-based decline in appetite, the forum was told. Conservatively, starter pigs could accept a DON rate of up to 400 parts per billion, but the actual non-effect threshold may be somewhat lower on many occasions in practice due to such considerations as the other compounds present and the degree to which toxins were free or conjugated. The question was asked, could the appetite drop be mitigated by adding a flavour to the piglet's feed? Sometimes this is successful, came the reply, but not always.
Regular checks were advised to determine whether mycotoxin contamination of ingredients or complete diets had exceeded pre-set limits. Analyse before you attempt to treat the diet such as with an inhibitor, said advisers. Even where you decide a treatment of some sort is worthwhile, re-check contaminant rates at intervals afterwards to be sure you are not spending the money unnecessarily.
Not every herd can follow the example of the Norwegian unit by discarding a ration entirely as damaged by moulds. Inactivation of the toxins by a treatment may also be unavailable in time. In those conditions think of a cascade of potential uses, forum speakers indicated. Remember those sensitivity ratings, with pigs before other species and piglets before mature breeding stock. Use them to pass a piglet feed along to sows. A diet that is too contaminated even for them may still be acceptable to ruminants.