2.Kontrol suhu dalam ruang brooder
3.kontrol suhu luar brooder
4.Rapatkan tirai dalam,tirai luar dan plafon
5.Atur ketebalan sekam
The FDA rules affect the purchase of chicks and young hens, sanitation in production facilities, testing for the bacteria, and storage of eggs at farms with at least 3,000 laying hens. An FDA announcement states the rules are expected to reduce the number of S enteritidis infections by 60%, preventing about 79,000 cases of foodborne illness and 30 deaths annually.
The FDA also estimates the measures will decrease human health care costs and improve quality of life for consumers but cost egg producers about $81 mln annually.
Dr. Charles L. Hofacre, secretary-treasurer for the American Association of Avian Pathologists, said the FDA rules institutionalise practices that have reduced S enteritidis contamination in most of the industry, and he does not expect the regulations will have much impact on public health or on egg producers.
"For the table egg industry, it'll be a very good way for them to showcase what they've been doing over the last few years," Dr. Hofacre said.
Egg farmers began working with states and the United Egg Producers to develop quality assurance plans after S enteritidis contamination peaked in the late 1980s, Dr. Hofacre said. For companies that have not adopted measures similar to the new regulations, their most notable changes will likely relate to increased record keeping.
The regulations are published in a final rule that took effect on 8 September. Producers with more than 50,000 laying hens need to comply with the rule by July 2010, and those with more than 3,000 laying hens but fewer than 50,000 must comply by July 2012. The rules are expected to affect producers accounting for 99% of the nation's egg production.
To comply with the new federal requirements, most egg producers must do the following:
- Have and implement a written S enteritidis prevention plan and document compliance.
- Buy only pullets tested for S enteritidis contamination or raise pullets under monitored conditions.
- Implement biosecurity and pest control programmes.
- Clean and disinfect poultry houses with positive S enteritidis test results.
- Refrigerate eggs at 45 F (9.44 C) during storage and transportation.
- Conduct environmental tests for S enteritidis and test eggs following positive environmental tests.
- Keep records related to flocks for one year after the flocks are permanently taken out of production.
- Make records available to the FDA within 24 hours of an official request.
- Producers must register with the FDA, which the Federal Register notice states will help the agency with annual inspections and resource allocation.
Dr. Hofacre said the regulations were the result of a few companies' refusal to cooperate with the FDA and self-regulate to avoid egg contamination. He said it is unfortunate that a few producers' actions led to increased regulation, but he does not disapprove of the new rules.
Dr. Eric N. Gingerich, a diplomate of the American College of Poultry Veterinarians and a staff veterinarian and adjunct assistant professor at the University of Pennsylvania's School of Veterinary Medicine, expects his state's diagnostic laboratory system will need more-sensitive equipment and more staff members to handle the final rule's requirements. He also expects an increase in material costs associated with laboratory tests.
"The cost, according to our lab people, is going to be significantly higher for Pennsylvania producers—say, three times higher—for either the manure swab tests or the egg tests," Dr. Gingerich said.
He estimates materials will cost $35 for each manure drag swab and $36 for each egg test. Producers using the Pennsylvania state laboratories pay for the cost of materials, but not labor costs, he said.
However, he said a United Egg Producers figure indicates eggs will cost consumers only about one cent more per dozen under the new rules.
Dr. Gingerich still has questions about what producers should do after positive test results in areas where there are no buyers of pasteurized eggs, what training is planned for implementation of the rule, and whether recalls will be required following positive test results.
While Dr. Gingerich thinks the tests will remove some S enteritidis-positive eggs from the market, he said egg producers have largely gained control over the bacteria since the FDA rule was proposed in 2004.
The FDA proposal was similar when introduced in September 2004, and the agency held public meetings in 2004 and accepted comments through July 2005. The 2004 proposal and the 2009 final rule were developed as part of a series of farm-to-table egg safety efforts that the FDA and the Department of Agriculture's Food Safety and Inspection Service started in the 1990s, the Federal Register entry states.
Source: American Veterinary Medical AssociationKlik disini untuk melanjutkan »»
By Trevor K. Smith, Professor, Department of Animal and Poultry Science, University of Guelph, Ontario, Canada
Do you know that mycotoxins are the second most important issue faced by the animal industry today next to feed cost? This sentiment was expressed by 30 animal industry leaders, representing 15% of world feed production, who recently attended Alltech's President Club.
Mycotoxins are metabolites produced by fungi (moulds) that can infest crops pre-harvest and can continue to flourish under sub-optimal storage conditions. Grains with high moisture content are particularly unstable and prone to mould proliferation and possible mycotoxin production. Excess rainfall at harvest and at key periods during the growing season can be a major promoter of mycotoxin contamination of feedstuffs.
Aspergillus mainly in tropics
The most significant species of mycotoxin-producing fungi that have an impact on poultry production would include Aspergillus and Fusarium. The most significant mycotoxin produced by Aspergillus fungi are the aflatoxins. The fungi that synthesise aflatoxins A. flavus and A. parasiticus are considered to be tropical or semi-tropical moulds that thrive under conditions of high moisture and temperature. The effects of feed-borne aflatoxin on poultry production have been extensively studied and we have a good understanding of the tolerance of various classes of poultry. This is partly due to concern for human health and food safety issues arising from contamination of poultry products with aflatoxin, since aflatoxin is a potent hepatocarcinogen. Analytical techniques for aflatoxin analysis in feeds are very practical due to the small number of different compounds that allow their simultaneous analysis.
Another important mycotoxin is the nephrotoxin ochratoxin A. This compound is produced by Aspergillus ochraceus and Penicillium verrucosum. As with aflatoxin, there is concern that residual ochratoxin A in poultry products could pose a threat to human health due to the possible carcinogenic nature of this compound.
Fusarium in temperate climates
Fusarium fungi flourish in more temperate climates. Our understanding of Fusarium mycotoxicoses in poultry is much less complete than our understanding of aflatoxicosis. This is in part because of the very large number of Fusarium mycotoxins, more than 100 that have been chemically characterised, which makes complete analysis of feedstuffs for Fusarium mycotoxins impractical, if not impossible.
The most commonly recognised Fusarium mycotoxins include the trichothecenes, a large family of structurally-related compounds including deoxynivalenol (DON, vomitoxin), T-2 toxin, nivalenol, diacetoxyscirpenol (DAS) and over 100 others, zearalenone, an oestrogenic compound, fumonisins and fusaric acid.
Analysis in poultry feeds
A major source of error in mycotoxin analysis is inadequate sampling of feedstuffs, with sampling accounting for approx. 82% of the variability in analysis. Proper sampling protocols have been developed and published in an effort to minimise this source of error. However, even with such protocols, error is unavoidable as mycotoxins are not evenly distributed within a batch, but occur in hotspots. Even with correct sampling, as an example, from a 25 t batch of feed, approx. 100 sub-samples should be taken comprising a total of 25 kg. From this a 250 g sub-sample is taken and eventually a 1 g sample analysed. Considering that only 1 g is analysed from 25 t, it is hardly surprising that mycotoxin analysis is not accurate!
Another source of error is the potential presence of different chemical forms of mycotoxins that may escape routine analysis. Attention has been focused on the presence of conjugated forms of mycotoxins that are produced by plants. This may be the result of detoxification of mycotoxins by plant metabolism, and it has been suggested that the presence of conjugated mycotoxins might be used in genetic selection of plant resistance to fungal invasion. Although conjugated forms of dexoynivalenol (DON, vomitoxin) were identified many years ago (1992), little information is available regarding the relative significance of conjugated and free mycotoxins in poultry diets. Schneweis and co-workers identified glucose conjugated zearalenone insamples of wheat. Naturally-contaminated wheat and corn samples from Slovakia have been found to contain glucose-conjugated DON with up to 29% of deoxynivalenol in a glucose conjugated form (2005). More recently, an increase in DON concentrations of up to 88% were found when barley samples from North Dakota were treated with trifluoroacetic acid prior to analysis. Such acid treatment would hydrolyse all different conjugates of DON. Similar acid treatment of different barley samples showed up to 21% of total DON found in conjugated forms. Most recently, even higher levels of bound DON were found in barley and beer using a variety of analytical techniques.
Correct values underestimated
The frequency of bound fumonisin routinely exceeded free fumonisin in samples of European corn and corn-based foods. It is not yet clear if the conjugated forms of mycotoxins are as harmful to poultry as the parent compounds, but it has been shown that some conjugated mycotoxins can be hydrolysed in the digestive tracts of animals.
It must be concluded that until we have a better understanding of the frequency, toxicity and nature of conjugated mycotoxins, current mycotoxin analysis of poultry feeds should often be considered to be an underestimate of correct values. To further complicate matters, there exists a number of different analytical techniques (for example ELISA and HPLC) that vary in accuracy and can be sensitive to interference from some dietary components (such as in DDGS). It should also be noted that typically feeds are only analysed for the presence of certain ‘indicator’ mycotoxins. It is well established that mycotoxins rarely occur in isolation and that mycotoxins, when present in combination, can act synergistically to produce more pronounced detrimental effects in the bird. It is necessary at this time, therefore, to consider mycotoxin analysis of feeds as offering only an approximation of the true hazard posed by the feeding of contaminated materials to poultry.
Effects on performance
A series of studies has been conducted to determine the effects of feeding blends of naturally-contaminated feedstuffs, largely corn and wheat, to different types of poultry. This was done in an effort to mimic conditions seen in commercial poultry production where diets contain multiple vectors of mycotoxin contamination. The mycotoxinsin such diets were determined to be mainly DON with lesser amounts of zearalenone and 15-acetyl DON in addition to fusaric acid. Three different modes of action of the mycotoxins fed were identified: reductions in cellular protein synthesis; reduced immunity; and alterations in brain neurochemistry.
Reductions in cellular protein synthesis result in lesions of the gastrointestinal tract, including necrosis, gizzard erosion, haemorrhaging, and malabsorption of nutrients. Reduced hepatic protein synthesis can decrease utilisation of dietary amino acids resulting in increased uric acid synthesis as amino acids are oxidised for energy purposes.
Many Fusarium mycotoxins, as well as aflatoxin and ochratoxin, have been shown to be immunosuppressive. This results in increased susceptibility todisease, lingering health problems in theflock and possible failure of vaccination programmes. The disease symptoms arising from immunosuppression, moreover, are not symptoms characteristic of mycotoxins. They are only indirectly caused by mycotoxins and this makes certain identification of mycotoxins as the causative agent of reduced flock health very difficult.
Combinations of feed-borne Fusarium mycotoxins are pharmacologically active. This means they have drug-like properties due to their effects on brain neuro-chemistry. The most reproducible effects observed are elevations in brain regional concentrations of serotonin. Such changes alter behaviour, including reductions in feed intake, loss of muscle coordination and increased lethargy. The effects on various types of poultry were as follows:
The feeding of a blend of ingredients naturally-contaminated with a combination of Fusarium mycotoxins resulted in reduced growth in the grower phase, elevations in blood uric acid levels, discoloration of breast meat and immunosuppression. Other research also showed changes in brain neurochemistry.
The feeding of a similar combination of Fusarium mycotoxin contaminated materials to broiler breeders significantly reduced hatchability due to reduced shell thickness of fertile eggs. Changes in brain neurochemistry were also observed. There were no effects of diet on sperm quality. In a parallel study with broiler breeder pullets, Girgis and co-workers observed immunosuppression.
Laying hens were very sensitive to the feeding of combinations of Fusarium mycotoxins. Egg production and feed efficiency were reduced while major increases in blood uric acid concentrations were seen. The elevations in blood uricacid levels were likely due to a reduction in hepatic fractional protein synthesis rates. Immunosuppression was also observed.
Turkeys were very sensitive to the feeding of high levels of Fusarium mycotoxin-contaminated feeds. Growth rates were significantly reduced even in the starter phase (Table 1) and some indices of immunosuppression were seen. The feeding of lower concentrations of Fusarium mycotoxins also reduced growth rates, elevated blood uric acid levels and caused immunosuppression. This was coupled with morphological changes in the small intestine and changes in brain neurochemistry.
Ducks were quite resistant to the feeding of combinations of grains naturally-contaminated with Fusarium mycotoxins. Indices of immunosuppression, however, were observed.
It can be concluded that poultry are sensitive to combinations of feed-borne Fusarium mycotoxins and that the feedingof contaminated materials should be minimised. It appears that the frequency of mycotoxin contamination of poultry feeds is increasing. This may be due in part to adverse weather conditions pre-harvest in many parts of the world arising from global climate change. The complex nature of modern poultry rations including the increasing use of potentially contaminated by-products such as distillers’ dried grains adds to the possibility of toxicological synergy between combinations of mycotoxins, thereby increasing the severity of the response of poultry to contaminated feeds. Many of the adverse effects seen in the studies reviewed above could be prevented by the simultaneous feeding of a polymeric glucomannan mycotoxin adsorbent (Alltech Inc.). The use of an appropriate mycotoxin adsorbent is likely the best short-term strategy available for minimising the adverse effects of feed-borne mycotoxins in poultry feeds. It is hoped that long-term strategies such as improved quality control measures arising from advances in analytical methodology and plant breeding strategies to reduce the susceptibility of plants to fungal invasion will help to minimise mycotoxin challenges to the poultry industries in the future.Klik disini untuk melanjutkan »»
The survey showed that campylobacter was present in 65% of the samples of chicken tested. Salmonella was in 6% of samples, 0.5% of these samples contained S. enteritidis and S. typhimurium.
Andrew Wadge, Director of Food Safety at the Food Standards Agency, said: "The continuing low levels of salmonella are encouraging, but it is disappointing that the levels of campylobacter remain high. It is obvious more needs to be done to get these levels down and we need to continue working with poultry producers and retailers to make this happen. Other countries like New Zealand and Denmark have managed to do so; we need to emulate that progress in the UK."
As part of the Agency’s work to reduce levels of campylobacter in UK-produced chicken an international conference on campylobacter is being organised for 2010, where a range of options for tackling the bug will be discussed.
Campylobacter is the most common bacterial cause of food poisoning. It is responsible for around 55,000 cases of illness in the UK every year, and is therefore one of the key organisms the Agency is tackling in order to reduce levels of foodborne illness. Campylobacter can be found on meat, unpasteurised milk, and untreated water; however there is strong evidence that chicken is the most common cause of illness.
The FSA emphasises that while campylobacter is still present in a significant proportion of fresh chicken sold in the UK, cooking chicken properly all the way through will kill the bug, so consumers can avoid the risk of illness.
The UK-wide survey of fresh chicken at retail was carried out between May 2007 and September 2008. During the course of the survey, 3,274 samples were tested for the presence of campylobacter and salmonella.Klik disini untuk melanjutkan »»