FDA: new rules to reduce Salmonella from eggs

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FDA: new rules to reduce Salmonella from eggs 21 Sep 2009

New federal regulations require most egg producers to take steps to prevent the spread of Salmonella enteritidis, reports the American Veterinary Medical Association.

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 Association

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Salting the birds before slaughtering

Heat stress is known to lead to poor performance and mortality. However, the reasons for that are varied and not so clear-cut. Acid-base imbalance may play a significant role here. Taking care of it can thus help us to deal with the problem, besides being important on its own.

By Dr Rogério G. T. da Cunha, Sao Paulo, Brazil

Keeping birds in a thermal comfort state is now widely known to have a significant impact on performance. Less acknowledged, though, is that an adequate internal pH is equally important for productivity. Even less known is that the two may have a significant link. Interestingly, the management of electrolytes in the diet can help us to "kill two birds with one stone". Dr Sebastião Aparecido Borges, professor at Universidade Tuiuti do Paraná, and André Favero (Master’s student at UFPR – Federal University of Paraná, Brazil) dissected these issues in a paper they presented at a poultry event.

Acids, bases and salts

Borges explains that the body attempts to maintain its pH, or acid-base balance, through the control of the ions H+ and HCO3-. These are produced by the dissociation of carbonic acid (H2CO3), which, on its turn, is formed by the combination of carbon dioxide (CO2) and water (H2O). The body also needs to keep electrolytes at appropriate and reasonably constant levels, the so-called electrolytic balance. For that end, he reminds that the sum of positively charged ions, like sodium and potassium, needs to be the same as the sum of the negative ones, such as chloride. Besides, each one of the ions has a narrow range of optimal values for its bodily concentration.

However, the two aspects are closely interconnected. "An acid-base imbalance makes the control of electrolyte levels by the body more difficult, and can lead to an imbalance of them as well, and the other way round," says Borges, adding that heat stress plays a role as it leads to an acid-base imbalance. "In very simple terms the panting, which is an attempt of the bird to cool itself, leads to the loss of water and carbon dioxide. This takes H2CO3 from the body, which then removes H+, thus increasing the pH, a process called respiratory alkalosis."

On a cascade of consequences, there is an increase in water consumption, a decrease in feed intake, prostration, and an impact on the electrolytic balance, with some ions being lost in the urine.The electrolytic and acid-base imbalancesmake internal conditions for the entire physiological machinery of the body far from ideal. All of this has an obvious impact on zootechnical indexes and may even lead to death.

Spicing them up

Given the relationship between electrolytic and acid-base balance, scientists began to consider ways to play around with them. Even more interesting, they began to wonder if they could not get round heat stress concerns. According to Borges, the main idea is to correct acid-base imbalance through the administration of salts, which break up in electrolytes. "This way we fight the loss of some ions, and also stimulate water consumption. This reduces the temperature of the bird, which in turn decreases panting, thus stabilising the pH. Both electrolytic and acid-base balances are maintained," Borges explains.

Nonetheless, things are not as simple as merely throwing some salts in the feed. Borges recalled that it was found that giving too much salt or giving them at wrong concentrations has adverse effects. The concept of interest here is the electrolytic make-up of the feed. In theory, we should take into consideration all the ions for its calculation. However, working with the most important ones in terms of bodily concentration (sodium, potassium and chloride) is enough for our purposes. In that case, a simple formula (mEqNa + mEqK – mEqCl) describes the electrolytic make-up of the feed. He explains that if such relation is too high, the birds end up drinking too much water. This leads to excreta that are more fluid and a wet bed. "It also causes alkalosis, while a very low relation leads to metabolic acidosis, which is a decrease in bodily pH. Furthermore, too much or too little of the component salts also causes problems," Borges details. In addition, the recommendations vary with the birds’ age and breeding purpose. Reviewing dozens of papers on the issue, and a few of his own team, he arrives at the recommendations in Table 1.

Cautions and precautions

One also needs to pay attention to individual ions. Borges recommends avoiding extreme levels of Na+ (below0.15% and above 0.45% in the formulation of the feed) and Cl- (above 0.70%). Among the most commonly used salts we have potassium chloride (KCl), sodium chloride (NaCl), sodium bicarbonate (NaHCO3), and potassium carbonate (K2CO3).

An alternative to the addition of salts to the feed is to provide them through the drinking water. Borges considers it a simple and effective way to give electrolytes to the birds, especially in heat stress situations. "It is also an interesting strategy to consider for stimulating water consumption in the pre-slaughtering fast. This decreases heat stress and dehydration, and their concurrent losses, also improving meat quality. One should not forget, though, that the total amount of electrolytes given to the birds must respect the limits above," he completes.

Despite being a strong advocate of the use of electrolytes, given that they do increase viability, improve zootechnical indexes, and fight the adverse effects of heat stress, Borges adds some words of caution. "Before considering the use of salts, it is of utmost importance that one knows the exact quantity that is already present in the other feed components, not to run the risk of going over the limits. We should pay close attention to our own results and tune or review our actions accordingly. Besides, this field is still under development. Topics that are yet to be more fully worked include: incorporating more ions to the recommendations; understanding the interplay between them; developing finer considerations about individual concentrations, and the form of administration through different salts. Thus, recommendations may change or new precautions may arise," Borges concludes.

World Poultry Vol. 25 No. 3, 2009

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MYCOTOXINS

The frequency of mycotoxin contamination of poultry feeds appears to be on the increase globally. This is a serious threat, since complex poultry rations are highly susceptible. As a result, such contamination can seriously affect bird performance. Proper measures are needed to minimise losses.

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:

Broilers

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.

Broiler breeders

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

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

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

Ducks were quite resistant to the feeding of combinations of grains naturally-contaminated with Fusarium mycotoxins. Indices of immunosuppression, however, were observed.

Minimise contamination

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.

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Campylobacter and Salmonella in chicken

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.

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Chicken sounds indicate stress

Ongoing research on laying hens has demonstrated that bird vocalizations can serve as reliable indicators of particular forms of stress and that different vocalization patterns can be linked with specific kinds of stressful conditions.

Knowing whether and when specific environmental conditions induce stress is a first step towards reducing stress in the production environment, according to Dr Michael J. Darre, a professor in the Department of Animal Science, University of Connecticut, and a member of The Poultry Science Association (PSA).

"Alleviating stress in commercial flocks of laying hens and broilers is important not only because it improves the overall welfare of the birds, but also because stress is a known enemy of production efficiencies," said Dr Darre. "Research involving the analysis of chicken vocalisations may well provide the answer, because it is non-invasive and provides immediate and accurate feedback on levels and types of bird stress."

The Dolittle Project

Joining Darre in his work on chicken vocalisations is one of his doctoral students, Ebenezer Otu-Nyarko. They are participants in a wider study called the Dolittle Project: Classifying Animal Vocalisations. Funded through the National Science Foundation, the Dolittle Project is the first ever to apply modern speech-processing algorithms to animal vocalisations. The lead investigator of the Dolittle Project is Dr Michael Johnson, a professor in Marquette University's Department of Computer and Electrical Engineering.

Chicken vocalisations as stress indicators

According to Dr Darre, one of the primary initial goals of the work on chickens was to determine if vocalisation patterns were the same for all types of stressors; research has shown that they are not. For example, vocalisation patterns have been found to be different for stress due to handling and stress due to overcrowding.

The analysis was carried out by digitally recording laying chickens' vocalisations under different types of stressful conditions, and then, after removing background noise, analysing the recordings using a modified version of the Hidden Markov Model (HMM) with voice recognition algorithms. The modified HMM is a statistical model developed by Marquette University that represents both the temporal and spectral characteristics of audio signals. When applied to chicken vocalisations, HMM has achieved an overall condition classification accuracy of 74%.

Darre and Otu-Nyarko are also looking at how vocal patterns change from the time chickens hatch until they are adults.

The ultimate goal of their work is to develop a "black box" that can be placed in chicken houses that allows farmers to remotely monitor their birds, notifies the farmers when it detects stress vocalisations, and identifies the type of stress, so that action can be taken immediately.

"This kind of monitoring would help reduce overall stress in flocks and be a great step forward in improving the welfare of commercial bird flocks. This in turn would benefit farmers, and ultimately the consumer, via improved egg-laying and meat output due to the known benefits that accrue from keeping chickens in a lower-stress environment," said Dr Darre.

Source: Poultry Science Association (PSA)

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Indonesian chicken gene resistant to bird flu

At least 62% of chickens indigenous to Indonesia are resistant to bird flu, thanks to a "Mx" gene in their body, the Indonesian Institute of Science (LIPI) revealed.

“Genetically, the indigenous chickens [to Indonesia] have a gene that is immune to avian influenza,” said head of the institute Umar Anggara Jenie, in an exposé of a biological study she gave at the Cibinong Sciences Center in Bogor, West Java, reports the Jakarta Post.

Sri Sulandari, a gene researcher at the institute’s biological research centre who studied the genes of indigenous chickens, said her institute carried out the first ever gene study focusing on how humans coped when contracting the virus and on the vaccination process. “Few have looked into the genetic side to see how chickens themselves have a natural resistance to bird flu. The indigenous chickens’ ability to resist avian influenza varies according to the strength of the antivirus genes in their body,” Sri said.

Recent evidence indicated the Mx gene was associated with chicken resistance or susceptibility to highly pathogenic bird flu. Sri says that Indonesia’s varied population of indigenous chickens is a mine of information on the Mx gene and how resistant each breed of chicken is to bird flu. She went on to say that if there is a bird flu epidemic in a certain region, it is unwise to simply cull indigenous breeds, as we may lose crucial information on the Mx gene.

Based on samples taken from 1,872 indigenous chickens of various breeds, the institute rated the dark-colored Cemani chicken the most resistant to the virus and the green forest chicken the most susceptible.

Source: The Jakarta Post

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Flies spread drug-resistant bacteria in poultry

Researchers at the Johns Hopkins Bloomberg School of Public Health in Baltimore, US, found evidence that houseflies collected near broiler poultry operations may contribute to the dispersion of drug-resistant bacteria and thus increase the potential for human exposure to drug-resistant bacteria.

The findings demonstrate another potential link between industrial food animal production and exposures to antibiotic resistant pathogens.

Previous studies have linked antibiotic use in poultry production to antibiotic resistant bacteria in farm workers, consumer poultry products and the environment surrounding confined poultry operations, as well as releases from poultry transport.

Vectors

“Flies are well-known vectors of disease and have been implicated in the spread of various viral and bacterial infections affecting humans, including enteric fever, cholera, salmonellosis, campylobacteriosis and shigellosis,” said lead author Jay Graham, PhD, who conducted the study as a research fellow with Bloomberg School’s Center for a Livable Future.

"Our study found similarities in the antibiotic-resistant bacteria in both the flies and poultry litter we sampled. The evidence is another example of the risks associated with the inadequate treatment of animal wastes."

“Although we did not directly quantify the contribution of flies to human exposure, our results suggest that flies in intensive production areas could efficiently spread resistant organisms over large distances,” said Ellen Silbergeld, PhD, senior author of the study and professor in the Bloomberg School of Public Health’s Department of Environmental Health Sciences.

Flies and samples

Graham and his colleagues collected flies and samples of poultry litter from poultry houses along the Delmarva Peninsula - a coastal region shared by Maryland, Delaware and Virginia, which has one of the highest densities of broiler chickens per acre in the US.

The analysis by the research team isolated antibiotic-resistant enterococci and staphylococci bacteria from both flies and litter. The bacteria isolated from flies had very similar resistance characteristics and resistance genes to bacteria found in the poultry litter.

Flies have ready access to both stored poultry waste and to poultry houses. A study by researchers in Denmark estimated that as many as 30,000 flies could enter a poultry house over the course of six week period.

Confined animal feeding operations

According to Robert Lawrence, MD, director of the Center for a Livable Future, confined animal feeding operations – where thousands of animals are crowded together and are fed antibiotics for growth promotion – create the perfect environment for selection of bacteria that are resistant to antibiotics.

“Antimicrobials are among the most important developments of the twentieth century in managing infectious diseases in people."

"We can’t afford to squander them by using them as growth promoters in industrial food animal production. The increase in antibiotic-resistant bacteria is a major threat to the health of the public, and policymakers should quickly phase out and ban the use of antimicrobials for non-therapeutic use in food animal production,” said Lawrence.

The study is published in the April 2009 issue of Science of the Total Environment.

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Enzyme technology key to profitable egg production

Layer producers looking for lower feed costs with higher fibre feed ingredients can use the latest developments in enzyme technology reported Dr Yingjun Ru at the VIV Asia Eggs conference, Thailand, Bangkok, 12 March 2009.
Using a carefully selected balance of xylanase, amylase, protease and phytase can reduce corn-based layer feed costs by more than $7.50/tonne.

The supply of more fibrous feed ingredients into the feed industry has increased with the growth of the bioethanol industry and increased demand for cereal grains into the food industry. Whilst these high-fibre ingredients are potentially a cost effective alternative, their use in layer feed can be limited by the low and often variable digestibility of nutrients.

Dr Ru, Regional Technical Services Manager, Danisco Animal Nutrition, presented a paper “Recent Advances in Enzyme Technology for More Profitable Egg Production” which outlined how the latest developments in enzyme technology can increase the use of high fibre ingredients into the feed formulation to achieve lower feed costs without depressing laying hen performance.

The paper summarised trials conducted in the Philippines and Australia where adding a combination of xylanase, amylase and protease enzymes (Avizyme® 1500, Danisco Animal Nutrition) allowed the nutrient specification of a corn-soy based diet to be reduced by 5% for energy, protein and amino acids without depressing laying hen performance.

In both trials, performance of layers fed medium specification (2610 kcal/kg or 2650 kcal/kg) corn-based diets containing higher levels of fibrous ingredients (wheat pollard or rice bran and copra meal) and supplemented with the enzyme combination were comparable to laying hens fed higher specification (2750 kcal/kg or 2775 kcal/kg) corn-based diets.

Adding new generation E. coli phytases (Phyzyme® XP, Danisco Animal Nutrition) provides egg producers with the opportunity to further reduce feed costs. A trial conducted at the Bangkok Animal Research Centre, Thailand supported using phytase to reduce the specification of the feed formulation for energy and amino acids as well as for calcium and phosphorus.

Dr Ru concluded that the key to more profitable egg production lies in combining and optimising enzyme activities according to the feed ingredients used in the formulation.

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Necrotic enteritis

Causes: Necrotic enteritis is caused by Clostridium perfringens types A or C. The organism is transmitted by soil, dust, litter and faeces. Can be induced by choice of raw materials in feed and/or coccidiosis. Clostridium perfringens can become especially prevalent in the small intestine when no antibacterial growth promoters are used.

Effects: Ataxia, intoxication, diarrhoea, depression, ruffled feathers, reluctance to move. It may also cause dysbacteriosis, leading to vitamin or mineral deficiency.

Detailed causes:

All types of chickens from two weeks onwards are susceptible to this acute to chronic disease. The agent involved in the aetiology of the disease is Clostridium perfringens which produces types A and C alpha toxin and type C beta toxin. It is also called creepers because chickens are sometimes ataxic (can’t move).

Mode of transmission

Soil, dust, litter and faeces spread the organism.

Special note

It may cause malabsorption syndrome leading to vitamin or mineral deficiency.

Clinical signs:

Ataxia, intoxication, diarrhoea, depression, ruffled feathers and reluctance to move may be seen.

In acute cases death can occur within hours of the disease onset.

Postmortem lesions

Dehydration (darkened skin), emaciation (no breast muscle), congested liver, cooked (ruffled up) intestinal mucosa – primarily of the jejunum and ileum can be seen. Intestines are often distended and filled with gas. There is water in the crop.

In acute cases enteritis occurs with just a grey layer of necrotic material on the mucosa.

Diagnosis:

Diagnosis is based on the gross lesions (ruffled intestinal mucosa), clinical signs and bacterial isolation on blood agar plate. Colonies are surrounded by an inner zone of complete haemolysis and an outer zone of discolouration and incomplete haemolysis.

It simulates coccidiosis and ulcerative enteritis.

Treatment and control:

Prevention

Bacitracin 50 g/ton given continuously in the feed, improved sanitation, lincomycin in feed or water. Rearing birds on wire will prevent the disease.

Treatment

Bacitracin (200 g/T) in the feed and vitamins and minerals in the water to reduce the disease.

Lincomycin, ozytetracycline, amoxicillin and tylosin can also be used to treat the disease.

Note

Bacitracin is now banned in most countries.

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Haemorrhagic enteritis (HE)

Causes: HE virus is a double stranded DNA Adenovirus.

Effects: Incubation period is less than 24 hours. Depression, bloody droppings, dark red to brownish blood on the skin and feathers around the vent can be seen. Mortality is 10-80%.

Detailed causes:

Turkeys of 4 weeks or older may develop this acute viral disease. HE virus is an unenveloped, icosahedral, double-stranded DNA virus. It replicates in the nucleus forming basophilic inclusion bodies (viral factories seen under light microscope).

Mode of transmission

Spreads orally from infectious faeces or litter.

Clinical signs:

(Incubation period is less than 24 hours).

Depression, bloody droppings, mortality (10-80%), dark red to brownish blood on skin, feathers and around vents can be seen.

Postmortem lesions

The skin and flesh are pale, anaemic and dark in colour.

The jejunal mucosa is read and highly congested, spleens are enlarged, friable and mottled, lungs are congested and vascular organs are pale, and the livers are enlarged with haemorrhage.

Diagnosis:

Clinical signs, and gross and microscopic pathology are useful.

Intranuclear inclusion bodies in the reticuloendotheial (RE) system and intestine are diagnostic.

Spleens show RE hyperplasia and inclusion bodies. ELISA or AGP tests can be used to detect antibody.

Treatment and control:

Prevention

Use of a live vaccine in drinking water at 4 and 6 weeks of age can prevent the diseases.

Treatment

None.

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Cannibalism

Occurrence: Worldwide.

Species affected: All.

Age affected: All.

Causes: Predisposing factors include insufficient feed or feeder space, high density rearing, excessive light, too much heat, nutritional deficiencies or irritation from external parasites.

Effects: Injuries to the vent, head or feet, missing feathers. Injuries can be severe.

Detailed causes:

Predisposing factors include insufficient feed or feeder space, high density rearing, excessive light, too much heat, nutritional deficiencies or irritation from external parasites.

Clinical signs:

The following are common forms of cannibalism seem in commercial poultry operations:

Vent-picking

Picking of the vent or region of the abdomen several inches below the vent is the most severe form of cannibalism. This is generally more common in high-production or overweight pullet flocks. Predisposing factors are prolapse or tearing of the tissues by passage of an abnormally large egg. Vent picking can result in anaemia.

Feather-pulling

Frequently seen in flocks kept in close confinement resulting in lack of sufficient exercise. Nutritional deficiencies may contribute to the problem.

Toe-picking

Most commonly seen in young birds. Inadequate feeder space or inability of the chick to find the feed will lead to toe-picking.

Head picking

Follows injuries to the comb or wattles.

Diagnosis:

Injuries seen around the head, vent and feet, or observation of cannibalistic activity are indicative.

Treatment and control:

Prevention

Provide adequate feed and feeding space, reduce bird density, reduce light, beak trimming, toe and comb trimming in breeders and wattle trimming in cage birds. Coloured light can help to reduce the problem. Give "toys" for the birds to play with like straw, branches etc.

(beak trimming, toe and comb trimming and wattle trimming will soon be forbidden in Western Europe).

Chick feeder lids or paper should be filled with feed and be in place prior to the reception of the chicks.

Automatic feeders (pan-shaped or troughs) should be available no later than 7 days of age. Feed lids and automatic feeders should overlap by 3 days to ensure smooth transition between the two feeding systems.

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Colibacillosis

Occurrence: Worldwide.

Species affected: All.

Age affected: All.

Causes: Gram negative bacteria- Escherichia coli. It is the most common bacterial pathogen of poultry, and the second most common of all poultry pathogens.

Effects: Low performance in older birds, or high mortality in younger birds. High embryonic mortality, respiratory distress and enteritis can be evident.

Detailed causes:

This disease has a number of names because it causes granulomas in adults and yolk sac infection in chicks.

Coli Granuloma is chronic in mature birds of all species, and may be acute in chicks occurring as omphalitis.

Escherichia coli are gram-negative, non-acid-fast, non-spore-forming bacilli, and many strains have flagella.

Mode of transmission

E. coli may be a primary or secondary invader. It is the most common bacterial pathogen in poultry and second most common of all pathogens of poultry.

Faecal contamination of eggs, transovarian contamination, contaminated water and feed with bacteria can occur commonly.

Aerosol spread may occur.

Special note

E. coli is a normal contaminant in the intestines and may complicate mycoplasma, IBV, LT, and/or NDV in the air sacs, heart, liver and lungs causing air sacculities and/or chronic respiratory disease (CRD). Several serotypes make vaccination difficultur. E. coli is a very important cause of economic losses in poultry due to mortality, drops in weight gain, hatchability and an import cause of Septicemia-toxemia (sept-tox), air sacculities, and IP condemnations in processing plant. Sept-tox is the leading infectious cause of condemnation in the broiler processing plant in the US, air sacculities is the second, and IP the third.

Clinical signs:

Low performance in older birds or high mortality in younger birds, high embryonic mortality, respiratory distress and enteritis (diarrhoea) can be evident.

Postmortem lesions

Cauliflower-like nodules on viscera (granuloma), omphalitis in chicks, discoloured and misshapen yolk (mushy chick) are seen. These lesions are characteristic. Air sacculitis, salpingitis (inflammation of the oviduct), enteritis, synovitis, arthritis, pericarditis, peritonitis, panophthalmitis, or swollen head syndrome are common. Cellulitis, an inflammation of the cellular or connective tissue, can be caused by E. coli. The soft tissue is heavily necrotic and may be gangrenous. It can result in extensive processing plant condemnation. It is sometimes called infectious process or IP.

Diagnosis:

Laboratory isolation of E. coli for lesions, yolk, blood on MacConkey’s or methylene blue agar (EMB). Colonies are pink on MacConkey’s and dark with metallic sheen. It simulates Salmonella, Staphylococcus, Tuberculosis, Fowl cholera, Marek’s disease and Aspergillosis.

Treatment and control:

Prevention

• Use mycoplasma-free stock to prevent interaction with E. coli.
• Pellet feed to kill bacteria.
• Bacterin for breeders or turkeys (serotype 02, 078) egg and hatchery sanitation to reduce organisms.
• Chlorinate water (3 to 5 ppm) and use nipple drinkers to reduce transmission in water.
• An inactivated vaccine is available for breeders and layers.

Treatment

Chlortetracycline (CTC) (400 g/ton), Oxytetracycline (OTC), Quinolones (Flumequine), Sulfadimethoxine and Ormetroprim or Trimethoprim, can be used.

Gentamicin can be given by subcutaneous injection at 1 day-of-age.

Chlorox® in water at 2 to 4 oz/gal for 1-3 weeks or Quinolone in water for 3-5 days to treat clinical signs.

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Aspergillosis

Causes: Fungal infection caused by Aspergillus fumigatus, A. flavus and A. niger.

Effects: High mortality, respiratory distress, central nervous dysfunction, sleepiness, inappetance and emaciation. Conjunctivitis and cloudy eyes can be seen.

Detailed causes:

Aspergillosis is mainly seen in young birds as an acute disease. Chronic disease occurs in adults. The fungi Aspergillus fumigatus, A. flavus and A. niger are responsible. It spreads by the aerosol spread of spores, which are common in the hatchery, and less commonly by contaminated dust and litter in the house.

Clinical signs:

Signs include high mortality, respiratory distress (dyspnoea and gasping), central nervous dysfunction (tremors, ataxia, and torticollis) somnolence (sleepy), inappetance, and emaciation (very thin), conjunctivitis and cloudy eyes can be seen.

Postmortem lesions

Yellowish-green or whitish, caseous (cheesy) nodules and/or green, fur-like down in mouth, palate, lungs, trachea, syrinx, viscera, air sacs, brain and eyes may be seen.

Diagnosis:

Fungus can be identified microscopically (20% KOH stain) from culture or special stain of tissues (hyphae, mycelia, conidophores). Isolation of culture in 48 hours on Sabouraud dextrose agar is diagnostic. Stain colony with lactophenol cotton blue to see conidophores. It is similar to colibacillosis, MD, and lymphoid leukosis. Nodules in the lungs and fungal fur-like down in the air sacs are diagnostic.

Treatment and control:

Prevention

Hatchery sanitation includes regular fumigation of eggs, machines and air ducts and regular (monthly) plating of hatchery with media to examine for the presence of fungi. Use clean dry litter and dry cups of nipples to reduce water spills. Quality of the feed is important. An aerosol of thiabenidazole or Clinafarm® pellets can be placed in the hatchery to kill fungus. Formalin fumigation is an effective method to kill Aspergillus in the environment (not in the chicken). This is not allowed in most of the USA.

Treatment
Quaternary ammonium, chlorine, and/or copper sulphate can be added to the water to help reduce the spread of the organism and reduce clinical signs. However, taking preventative measures is more effective.

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Sekilas Newcastle disease

Newcastle disease (ND) merupakan penyakit pernapasan dan sistemik, yang bersifat akut dan mudah sekali menular yang disebabkan oleh virus dan menyerang berbagai jenis unggas. Pengamatan dilapangan menunjukkan bahwa pada setiap kasus ND selalu ditemukan gejala gangguan pernapasan walaupun dalam bentuk campuran dengan gejala gangguan pencernaan ataupun gangguan saraf.
Penyakit ini dikenal juga dengan berbagai nama, yaitu pseudofowl pest, pseudovogel pest, atypishe geflugelpest, pseudopoultry plaque, avian pest, avian distemper, ranikhet disease, tetelo disease, korean fowl plaque dan avian pneumoencephalitis.
Berdasarkan atas gejala klinik yang timbul pada ayam, maka ND dapat dibagi atas 5 bentuk, yaitu Doyle, Beach, Beaudette, Hitchner, dan enterikasimptomatik.
Bentuk Doyle ditandai oleh adanya infeksi yang bersifat akut dan fatal pada ayam semua umur. Bentuk ini tersifat oleh adanya gangguan pencernaan akhibat perdarahan dan nekrosis pada saluran pencernaan sehingga dikenal dengan nama ND velogenik-viserotropik(VVND).
Bentuk Beach ditandai oleh adanya infeksi yang bersifat akut dan kerap kali bersifat fatal pada ayam semua umur. Bentuk ini tersifat oleh adanya gejala gangguan pernapasan dan saraf sehingga disebut ND velogenik-neurotropik.
Bentuk Beaudette merupakan suatu bentuk ND velogenik-neurotropik yang kurang patogenik dan biasanya kematian hanya ditemukan pada ayam muda. Virus ND penyebab infeksi pada bentuk ini tergolong tipe patogenik mesogenik dan dapat dipakai sebagai vaksin aktif untuk vaksinasi ulangan terhadap ND.
Bentuk Hitchner ditandai oleh adanya infeksi pernapasan yang ringan atau tidak tampak, yang ditimbulkan oleh virus dengan tipe patogenik lentogenik, yang biasanya digunakan sebagai vaksin aktif.
Bentuk enterik asimptomatik terutama merupakan infeksi pada usus, yang ditimbulkan oleh virus ND tipe lentogenik. Bentuk ini tidak menimbulkan suatu gejala penyakit tertentu.
Virus penyebab ND tergolong genus Avian paramyxovirus dan famili Paramyxoviridae, yang merupakan virus RNA yang mempunyai genom single standed dengan polaritas negatif. Paramyxovirus berbentuk sangat pleomorfik; biasanya berbentuk bulat dengan diameter 100-500nm, tetapi ada juga yang berbentuk filamen.
Paramyxoviridae terdiri atas 3 genera, yaitu Paramyxovirus, Morbilivirus dan Pneumovirus. Genus Morbilivirus terdiri atas mammalianderpest dan canine distemper. Genus Pneumovirus terdiri atas mammalian respiratory syncytial viruses, mouse pneumonia virus dan avian pneumovirus yang dihubungkan dengan swollen head syndrome (SHS). Genus Paramyxovirus terdiri atas virus mammalian parainfluenza, virus mumps dan avian paramyxovirus. Virus ND merupakan prototipe dari genus ini. Virus yang tergolong genus Paramyxovirus dapat dibedakan dari virus lainnya oleh karena adanya aktivitas neuraminidase yang tidak dimiliki oleh virus lain pada famili Paramyxovirus.
Penularan virus ND dapat terjadi secara langsung dari ayam salit ke ayam yang peka, tetapi dapat juga terjadi secara tidak langsung melalui bahan, pekerja atau alat yang tercemar virus tersebut. Ayam yang menunjukkan gejala gangguan pernapasan akan menyebabkan adanya udara bercampur titik air yang mengandung virus ND, yang berasal dari mukus ayam sakit. Dalam hal ini penularan virus ND dapat terjadi secara inhalasi. Virus ND yang terutama bereplikasi di dalam saluran pencernaan akan menyebabkan adanya feses yang tercemar oleh virus tersebut. Dalam hao ini, penularan virus ND dapat terjadi melalui oral akhibat ingesti feses yang mengandung virus tersebut ataupun secara tidak langsung melalui pakan atau minuman yang tercemar atau per inhalasi akhibat menghirup partikel feses yang telah mengering.
Pada infeksi alami, mas inkubasi ND berkisar antara 2-15 hari(rata-rata 5-6 hari). Kecepatan timbulnya gejala bervariasi menurut galur virus ND, jenis unggas, status kekebalan, adanya infeksi campuran dengan organisme lain, faktor lingkungan, rute infeksi dan dosis virus.
Pengobatan dengan antibiotik/antibakteri hanya bertujuan untuk mengobati infeksi sekunder oleh karena bakteri. Support multivitamin diperlukan untuk mempercepat kesembuhan jaringan yang rusak.

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Lalat...Si Pembawa Penyakit

Keberadaan lalat rumah yang disebut Musca domestica ini merupakan indikator kondisi sanitasi lingkungan. Demikian juga dengan dengan yang terjadi di lingkungan peternakan. Lalat yang beterbangan dapat dikatakan sebagai fenomena gunung es. Yang dimaksudkan adalah lalat dewasa yang kita lihat hanya 20% dari total populasi. Sementara yang 80% nya berada dalam stadia telur, larva dan pupa yang tersembunyi.

Sekali bertelur, seekor lalat rumah betina menghasilkan 100-150 butir atau 1000 butir seumur hidupnya. Dalam waktu 12-24 jam telur menetas dan berkembang menjadi larva dalam waktu 3-7 hari. Larva berkembang menjadi pupa dalam waktu 26 hari atau bahkan kurang dari itu, tergantung suhu lingkungan. Selanjutnya pupa menjadi lalat dewasa. Oleh karena kecepatan perkembangbiakannya, ada yang menyebut lalat sebagai an everyday monster.
Lalat termasuk dalam kelompok insekta, ordo Diptera, sub ordo Brachicera. Yang termasuk kelompok ini antara lain lalat kuda ( Tabanus) dan lalat rumah (Musca domestica).
Lalat rumah dianggap mengganggu karena kesukaannya hinggap di tempat-tempat yang lembab dan kotor. Selain hinggap, lalat juga menghisap bahan-bahan kotor dan memuntahkan kembali dari mulutnya ketika hinggap di tempat berbeda. Bisa dibayangkan pakan yang dihinggapi lalat akan tercemar oleh mikroorganisme baik bakteri, protozoa, telur/larva cacing atau bahkan virus yang dibawa dan dikeluarkan dari mulut lalat-lalat tersebut. Oleh karena itu lalat dianggap sebagai penyebar berbagai penyakit kepada manusia maupun hewan, antara lain demam typhoid, kolera, anthrax, tuberculosis, disentri, cacing gilig Ascaris dan cacing pita Raillietina. Bahkan menurut penelitian Prof. Dr. Hastari Wuryastuti dari Fakultas Kedokteran Hewan Universitas Gadjah Mada, lalat rumah diduga sebagai vektor atau penyebar virus Avian influenza. Penelitian tersebut belum selesai, masih memerlukan pembuktian lainnya. Namun pernah ditemukan bahwa lalat yang berasal dari farm yang terserang AI beberapa tahun yang lalu ternyata positif terdapat virus AI dalam tubuhnya.
Menyimak demikian banyak kerugian "memelihara" lalat rumah dalam kandang atau di dalam rumah maka lalat harus dihapuskan dari kedua lingkungan tersebut. Lalat betina menyukai tempat yang basah dan lembab dan mengandung protein seperti kotoran ayam sebagai tempat hinggap dan bertelur. Oleh karena itu sebaiknya kotoran ayam di kandang dalam keadaan kering yang dapat diperoleh jika penyerapan nutrisi dalam saluran pencernaan berlangsung optimal. Kondisi pencernaan demikian terjadi bila terdapat keseimbangan mikroflora usus dan bakteri di dalam saluran pencernaan.
Selain dengan menciptakan kotoran yang kering, pemakaian produk anti lalat juga banyak mengurangi populasi lalat. Ada produk yang ditaburkan di atas kotoran ada pula yang diberikan melalui pakan agar bahan tersebut ada di dalam kotoran dan membunuh larva yang akan berkembang menjadi pupa.
Selain lalat rumah, jenis lalat lain pun juga merugikan peternakan. Lalat Tabanus yang gigitannya menyakitkan dan mengiritsi kulit dapat berlaku sebagai penyebar penyakit surra. Lalat Gasterophilus bahkan "menitipkan" larvanya dalam lambung kuda sebelum dikeluarkan bersama dengan kotoran sehingga menimbulkan luka dilambung.
Bagaimanapun menjaga kebersihan termasuk merupakan langkaj yang cukup baik dalam rangka memutuskan siklus penyakit melalui lalat sebagai sang pembawa penyakit. Jangan sampai ada pakan yang tumpah dibawah kandang karena pakan mengandung protein yang disukai lalat untuk hinggap dan bertelur. Mari kita memerangi lalat!!!
Warta SANBE-VET no.36 Agustus 2008

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Pentingnya Aspirin dan Vitamin C

Busyet dah..ayamnya hari kemarin mati 23ekor!!!Kalo dilihat dari fisiknya dan hasil bedah ayamnya normal. Gak mau kecolongan, ayamnya dicek...dan ketemu ada ayam yang sedang telanjang. Ayamnya ngomong :"Bos..hawanya panas banget, pake kipas kurang nyess..jadinya buka baju..ehh buka bulu aja". Gitu kata ayamnya. Kesimpulannya, 23ekor mati akhibat stress panas. Ingin tahu gimana menanggulangi heat stress pada broiler, simak artikel dari Drh. Heri Setiawan berikut ini.

Secara umum suhu lingkungan bisa berfluktuasi antara 29'C hingga 36'C, dengan kelembaban 70-80 %. Kondisi tersebut tentu sangat tidak nyaman bagi ayam broiler. Fungsi normal organ-organ tubuh broiler akan mengalami gangguan sehingga terjadi penyimpangan proses metabolisme yang berimbas pada merosotnya produktivitas dan meningkatnya mortalitas. Ujung-ujungnya tentu saja kerugian.

Cekaman Suhu Panas (Heat Stress)

Apa yang sebenarnya terjadi di dalam tubuh broiler ketika suhu lingkungan begitu tinggi dan menimbulkan cekaman stress?Respon awalnya adalah menurunnya nafsu makan. Ini adalah respon yang logis dan mudah dipahami. Suhu lingkungan yang tinggi menyebabkan "penguapan air" dari dalam tubuh meningkat yang berakhibat konsumsi air minum bertambah. Reaksi selanjutnya lebih njlimet (tingkat kompleksitasnya tinggi) karena melibatkan rangkaian proses hormonal. Kortisol, hormon utama dalam kelompok glukokortikoid, berpengaruh paling besar pada metabolisme tubuh saat terjadi cekaman panas.
Tingginya kadar kortisol dalam darah mengakhibatkan atropi (pengecilan) pada organ-organ primer sistem imunitas. Suatu penelitian yang dilakukan di Lohare, Pakistan, membuktikan bahwa heat stress menyebabkan penurunan ratio berat bursa fabrisius, Thymus dan Limpa tehadap berat badan broiler. Meskipun secara histologis/mikroskopis tidak ditemukan kerusakan pada ketiga organ tersebut, namun terjadi penurunan daya imunitas. Berkurangnya daya tahan tubuh ini disebabkan oleh menurunnya kualitas (kerusakan/kelemahan) dan kuantitas (menurunnya produksi dan kematian) sel-sel B, T dan Limposit yang bertanggungjawab pada mekanisme kekebalan tubuh melawan penyakit infeksi.
Hormon lain yang ikut berpartisipasi pada mekanisme tubuh ketika terjadi heat stress adalah prostaglandin. Hormon ini menyebabkan terbentuknya penggumpalan sel-sel darah sehingga terjadi peningkatan viskositas (kekentalan) cairan darah. Akhibat selanjutnya adalah penyumbatan pada pembuluh darah, terjadi hipoksia (pasokan oksigen ke dalam sel menipis), metabolisme terganggu dan akhirnya terjadi hambatan pertumbuhan. Pada kasus-kasus yang berat, apalagi disertai komplikasi oleh mikroba pathogen, bisa berakhir dengan kematian dalam jumlah yang tinggi.

Pentingnya ASA

Lebih populer dengan sebutan Aspirin, ASA (Acetylsalicylic acid) mempunyai efek prostaglandi inhibitor. Disebut demikian karena ASA bisa merangsang dilatasi/pelebaran pembuluh darah dan mencegah terjadinya penggumpalan sel-sel darah. Efek positif yang nyata adalah normalnya metabolisme sel-sel tubuh karena lancarnya pasokan oksigen dan tidak terjadinya hipoksia. Hal ini dibuktikan dengan suatu penelitian pada sejumlah broiler yang dipelihara dalam kondisi hipoksia buatan. Broiler tersebut dibagi menjadi 5 kelompok dengan pemberian pakan berbeda. Kelompok 1 diberikan pakan tanpa ASA (kontrol). Kelompok 2-5 diberi pakan mengandung ASA dengan konsentrasi 0,025%;0,05%;0,1% dan 0,2%. Hasilnya: broiler dengan pemberian pakan mengandung 0,2% ASA menunjukkan hasil terbaik dibanding kelompok lainnya dalam mengatasi hipoksia. Produktivitasnya pun paling optimal.

Pentingnya Vitamin C

Dikenal sebagai anti stress, vitamin C berperan dalam metabolisme glukoneogenesis, yaitu suatu proses penyediaan energi selama terjadinya cekaman suhu tinggi. Mekanismenya melalui pengkonversian protein dan lemak menjadi energi untuk produktivitas dan bertahan dalam menghadapi stress tersebut. Selain itu vitamin C juga mengambil bagian dalam sintesa sel darah putih, khususnya sel makrofag dan netrofil, yang berperan dalam sistem pertahanan tubuh ayam. Suatu penelitian yang dilakukan di Kamboja menyimpulkan bahwa pemberian vitamin C pada broiler dengan dosis 40 mg/ekor/hari dalam air minum bisa mengurangi dampak negatif akhibat cekaman suhu tinggi. Produktivitas broiler tersebut meningkat yang ditandai dengan konversi pakan dan mortalitas yang menurun secara signifikan dibandingkan ayam kontrol (tanpa vitamin C) dan ayam yang diberi vitamin C dosis 20 mg/ekor/hari.

Pentingnya ASA dan Vitamin C

Gabungan ASA dan vitamin C ternyata menghasilkan efek sinergi yang berenergi. Saling memperkuat dan melengkapi dalam menghasilkan perlindungan pada ayam terhadap cekaman suhu tinggi. Penelitian di Lahore (Pakistan) yang dilakukan untuk mengetahui efek sinergiame bahwa pemberian gabungan ASA dan vitamin C pada broiler yang mengalami heat stress memberikan manfaat nyata, yaitu : membaiknya konversi pakan, status imunitas dan rasio berat bursa fabrisius, Tymus dan Limpa terhadap berat badan. Secara umum ASA dan vitamin C relatif aman. Dosis praktis yang dianjurkan pada kondisi lapangan dengan suhu lingkungan panas adalah 1 tablet ASA 500 mg dan 1 tablet vitamin C 500 mg dihaluskan kemudian dilarutkan dalam air minum untuk 50 ekor broiler umur 21 hari keatas. Hasil nyata terlihat bila diberikan pada tengah hari saat puncak terik matahari.
Nah..tunggu apa lagi, segera manfaatkan ASA dan vitamin C untuk menanggulangi dampak negatif suhu tinggi dan agar tidak ada ayam yang telanjang karena kepanasan.

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Apaan tuh Koksidiosis?

Kemarin sudah posting tentang Leucocytozoon, sekarang ganti Koksidiosis. Knapa koksidiosis?simpel aja alasannya, karena obatnya sama dengan Leucocytozoon,yaitu sulfamonodimetoksin atau sulfaquinoksalin.

Koksidiosis disebabkan oleh protozoa yang bernama Eimeria sp, penyakit ini bersifat diare dan enteritis (radang usus). Protozoa yang tergolong genus Eimeria memperbanyak diri di dalam saluran pencernaan dan menyebabkan kerusakan pada jaringan dan selanjutnya dapat mengakhibatkan gangguan pada proses digesti dan absorpsi nutrien, dehidrasi, kehilangan darah dan meningkatnya kepekaan terhadap penyakit lain. Koksidiosis terutama ditemukan pada unggas muda karena kekebalan akan cepat terbentuk setelah kontak dengan protozoa tersebut dan selanjutnya dapt memberikan perlindungan pada letupan penyakit berikunya. Meskipun demikian, ayam dewasa dapt terserang juga, hal ini mungkin karena tidak terdapat perlindungan silang antar spesies Eimeria pada unggas dan letupan berikutnya mungkin disebabkan oleh spesies Eimeria yang berbeda.
Kerusakan jaringan dan perubahan fungsi saluran pencernaan dapat mendukung adanya kolonisasi bakteri, misalnya Clostridium perfringens atau Salmonella typhimurium. Koksidiosis dapat mendukung timbulnya berbagai penyakit imunosupresif.
Secara alami, penyebaran Eimeria dapat dibatasi sendiri oleh protozoa tersebut dan terutama tergantung pada jumlah ookista yang ditelan dan status kekebalan ayam. Jumlah ookista di dalam litter atau feses ayam broiler paling tinggi pada minggu keempat sampai kelima, kemudian menurun pada periode berikutnya. Setelah ayam dipanen, biaanya hanya terdapat sejumlah kecil ookista yang dapat bertahan karena litter dan feses merupakan lingkungan yang tidak sesuai dengan perkembangan ookista.
Protozoa koksidiosis bersel satu, yang tergolong kelas Sporozoa, ordo Coccidia, famili Eimeriidae, dan genus Eimeria. Pada ayam telah dilaporkan 9 jenis Eimeria, yaitu Eimeria acervulina, Eimeria bruneti, Eimeria maxima, Eimeria mitis, Eimeria mivati, Eimeria necatrix, Eimeria praecox, Eimeria tenella, dan Eimeria hagani.Spesies Eimeria dapat diidentifikasi berdasarkan sifat-sifat yang spesifik, yaitu lokasi lesi pada usus, gambaran lesi makroskopik, ukuran, bentuk, dan warna ookista, ukuran skison dan merozoit, lokasi parasit di dalam jaringan, periode prepaten minimum pada infeksi buatan, waktu minimum untuk sporulasi, dan sifat imunogenisitas terhadat galur Eimeria yang murni.
Eimeria sp tidak menular secara langsung dari ayam satu ke ayam lainnya. Penularan alami koksidiosis hanya terjadi dengan cara menelan ookista hidup yang telah bersporulasi. Ayam yang terinfeksi dapat mengeluarkan ookista bersama feses selama beberapa hari atau beberapa minggu. Ookista yang terdapat di dalam feses akan menjadi infektif setelah proses sporulasi selama 2 hari. Penularan Eimeria antar kandang/peternakan dapat terjadi melalui pekerja atau peralatan yang berpindah-pindah. Ookista juga dapat berpindah melalui debu.
Gejala klinis koksidiosis bervariasi menurut spesies Eimeria yang infeksi ayam. Spesies Eimeria yang kurang patogen biasanya menyebabkan gejala klinis yang ringan atau tanpa gejala. Spesies Eimeria yang lebih patogenik dapat menyebabkan diare yang bersifat mukoid atau hemoragik. Gejala diare biasanya akan diikuti oleh dehidrasi, bulu berdiri, anemia, lesu, lemah, menekuk kepala dan leher, dan mengantuk. Lesi yang ditimbulkan oleh koksidiosis dapat dibagi berdasarkan lokasi lesi, yaitu sepertiga usus bagian depan disebabkan oleh Eimeria acervulina, sepertiga usus bagian tengah disebabkan Eimeria necatrix dan Eimeria maxima, sepertiga usus bagian belakang disebabkan Eimeria brunetti, dan sekum disebabkan Eimeria tenella. Meskipun demikian dapat terjadi tumpang tindih lokasi lesi pada usus yang ditimbulkan oleh berbagai jenis Eimeria.
Koksidiosis dapat ditanggulangi dengan sanitasi/desinfeksi yang ketat, menjaga kualitas litter yang optimal, dan penggunaan koksidiostat dalam pakan. Sampai sini info tentang koksidiosis, lain waktu akan saya sambung.

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Leucocytozoonosis

Description and Distribution

Leucocytozoonosis is a disease caused by a protozoan blood parasite transmitted by the bite of a blackfly (Simuliidae). Both wild and domestic avian species are susceptible to infection with Leucocytozoon species: L. simondi (ducks and geese), L. smithi (turkeys), L. bonasae (grouse and ptarmigan) and L. marchouxi (pigeons and doves). An unspecified species has been found in an osprey in Michigan. L. simondi has been implicated in major die-offs of Canada geese at the Seney National Wildlife Refuge, which occur approximately every 4 to 5 years, and is believed to be one of the major factors limiting the growth of the Seney Canada goose population. Die-offs generally occur in the spring (mortality may reach 100% in the goslings) but deaths due to leucocytozoonosis can be seen anytime during the blackfly season (May-August). In North America the distribution of L. simondi is the northeastern and northern midwestern U.S. and Canada. L. smithi infects both wild and domestic turkeys and is responsible for economic losses to the southeastern U.S. turkey growers. Leucocytozoonosis has not been demonstrated to be a disease problem in wild turkeys.

Transmission and Development

Leucocytozoon transmission begins each year with a spring relapse in previously infected birds. Birds with circulating elongate gametocytes are infective while those with circulating round gametocytes do not experience this relapse and are not infective. The circulating elongate gametocytes from the bird enter a blackfly during a blood meal. Sexual development takes place within the blackfly digestive system and sporozoites enter the salivary glands of the blackfly where they are injected into a susceptible avian host during a subsequent blood meal.

In ducks and geese, the development of L. simondi progresses through 2 asexual tissue stages, with initial hepatic schizogony developing into round gametocytes in red blood cells and later megaloschizonts found primarily in the spleen, developing into elongate gametocytes in white blood cells. The rupture of hepatic schizonts has been observed to occur around post exposure day 5 and rupture of splenic megaloschizonts occurs around day 10.

The appearance of both round and elongate gametocytes is related to the pathogenicity of the Leucocytozoon strain, with the more pathogenic forms progressing to the elongate stage. Circulating L. simondi gametocytes can be found in the bloodstream of infected birds from the time of spring relapse until early fall (April-September). In turkeys, L. smithi gametocytes persist in the bloodstream and may be found throughout the year, although in greatly reduced numbers during the winter months.

Clinical Signs and Pathology

The majority of birds affected with leucocytozoonosis exhibit no clinical signs. Those that are visibly affected show mild to severe signs of anorexia, ataxia, weakness, anemia, emaciation, and have difficulty breathing. Birds may die acutely at the time of hepatic schizont of splenic megaloschizont rupture, or chronically as a result of rupture of slower developing brain megaloschizonts. It is believed that the mortality in adult birds occurs as a result of debilitation and increased susceptibility to secondary infection.

Diagnosis

A diagnosis can be made by the demonstration of gametocytes in blood smears. Histopathological examination of the liver, spleen and brain can show developing Leucocytozoon megaloschizonts. Necropsy may reveal an enlarged spleen and liver. Since the majority of birds are subclinically infected with Leucocytozoon, other causes of death must be ruled out even with the presence of Leucocytozoon gametocytes in peripheral blood smears.

Treatment and Control

Control of the Leucocytozoon organism in domestic avian species has, until recently, been limited to control of the blackfly vector. Findings indicate that Clopidol (active ingredient in Coyden 25 coccidiostat - Dow Chemical Co., Midland, MI) may be useful in the control of leucocytozoonosis in domestic and wild waterfowl. Clopidol has been used successfully to control leucocytozoonosis in domestic turkey rearing operations in the southeastern U.S.

Significance

There is a potential for leucocytozoonosis outbreaks in waterfowl breeding grounds in the spring at Seney National Wildlife Refuge where severe losses may greatly depress population growth. Domestic duck rearing operations have been removed from parts of the northern Lower and Upper Peninsulas of Michigan due to leucocytozoonosis.

Leucocytozoonosis is of no public health significance since it is not infective to humans, and infected waterfowl are safe for human consumption.

www.michigan.gov

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