Raising paw quality with litter management

Footpad dermatitis (FPD) is a condition affecting broilers and turkeys and is also known as pododermatitis and paw burn, all of which refer to a type of contact dermatitis on the footpad and toes.

Before the mid 1980, chicken paws were of little value and were rendered with feathers, blood and other unslable portions. Chicken paws prices have skyrocketed because of an export demand for high quality paws, transforming this product into the third most important economic part, behind breasts and wings.

However, paws are downgradeed or condemned for a variety of reasons that include a condemned carcasses, plant machinery mutilations or FPD lesion. Roughly 99% of condemned paws are a result of FPD lesions. Not only is FPD a revenue loss, it is currently being used as an indicator of bird welfare in animal welfare audits. Improving foot health not only provides opportunity for increased profit from exportable chicken paws, but also ensures that the poultry industry continues to meet animal welfare standards.

Litter moisture

Recent work at the University of Georgia, USA, focuses on environmental factors-the relationship between litter moisture and depth and paw quality. Unfortunately, previous research has contradicting results. Some research has shown that paw quality is better with deeper litter and others have shown it is best with shallow depths. In this study, as litter depth increased, moisture decreased dan paw quality improved.

Wet litter can cause ulceration of broiler foot pads. Lesions have beed found to be more severe as litter moisture increases. Continuosly standing on wet litter causes the footpad to soften and become more prone damage, predisposing the bird to developing FPD. Drying out the litter and moving birds from wer litter to dry litter has been shown to reverse the severity of FPD.

Litter Management

Litter play as important role in moisture management. It acts as a sponge, absorbing moisture and allowing for the dilution of fecal material. Thicker bases of litter allow water retention and dissipation away from the surface where it comes into contact with birds. Litter must not only be able ti absorb lots of moisture, but should also have a reasonable drying time to get rid of that moisture.

Bedding material has become more expensive and, as a result, there are situations where inadequate amounts of shavings are placed in broiler houses. Litter sometimes may be spread unevenly throughout the house, being thicker in the middle than along the sides. Evenly spread out litter is critical to prevent ‘slicking over’ of the litter along the sidewalls. Ultimately the bedding material used depends on cost and availability. Regardless of the source of bedding, when possible use materials with smaller particle sizes, as they have been shown to produce better paws.

Litter management between flocks

If broiler houses are cleaned out between flocs, at least three to four inches of litter is need to handle the moisture. If on a bulit-up litter program, it is important to remove the caked litter to allow the litter base to dry before chicks are placed. Running fans during the day will remove moisture from the litter more rapidly.

Several methods are use to manage litter between flocks, such as tiling, removing cake and top-dressing and windrowing. Six commercial 40x500-foot broiler houses were used to evaluate how litter management in between flocks would influence the incidence of FPD. The three litter methods use were cake removal, complete cleanout and windrowing. Each treatment was applied to two houses. The result indicated tha the windrowed houses produced more Grade A and B paws in the processing plant than did caked and cleaned-out houses.

Drinker Management

Proper drinker line management according to manufacturer’s guidelines can prevent excessive moisture form being added to the litter. Drinkers that are too low or have the water pressure set too high tend to result in wetter floors. Water lines that may have a biofilm or other particulates can serusl in leaky nipples, which will also increase litter moisture. Regular flushing and sanitizing the drinker system will reduce water leakage. This will keep litter dried and improve its quality, subsequently resulting in better paw quality.

Managing the moisture undeneath the water and feed lines is essential because the birds spend the majority of their time in this area. Keeping litter dry in this area can reduce problems not only from FPD but also form hock and breast burns.

Ventilation

If relative humidity (RH) is not currently being monitored in broiler houses, it should be used as a house management tool. A main objective of minimum ventilation is to control house moisture, with the goal being to keep the RH between 50% and 70%.

More incidences of FPD and hock lesions have been observed in clod weather compared to warm weather and have a high correlation with relative humidity in the broiler house. These seasonal effects are related to the increased relative humidity in broiler houses that are because of reduced ventilation during cold weather. Circulation fans and attic inlets have been proven to promote dry floors in cold weather.

Bird density

The sudden onset of wet litter associated with higher bird densities in one area of a house compared to another is considered to have a large influence on the development of FPD. Litter conditions deteriorate as moisture increases with increased stocking density. As stocking density increases, water consumption per bird increases.

As bird drink more water, their feces become watery and contributes to overall litter moisture. One way to combat this is to properly use migration fences, even in cold weather months. Migration fences put in place after birds are released to the entire house from partial house brooding will ensure they are evenly spaced out, allowing for better litter management and temperature regulation.

One simple, cost effective way to monitor bird density is to add additional water meters. Water meters for the fron, middle and back of the house can indicate bird densities by simply looking at daily water consumption. Higher consumption in one end of the house means that there are more birds than in the other sections.

Make sure to have a dry litter base of at least three inches at the start of the flock to provide an adequate ‘sponge’ to handle the moisture. Proper housing and equipment management will allow for decreased RH inside the house and drier litter. Keeping litter drier can go along way to producing a healthier and more profitable flocks*****

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Infectious bronchitis virus: Range of viral strains makes control complicated

Infectious bronchitis (IB) has been reported as a disease only in chicken. All ages of chickens are susceptible to infection but the severity of the clinical disease varies. Infectious bronchitis is considered to be worldwide in distribution. The incidence is not constant trough the year,  being reported more of during the cooler months.

History

The disease was first described in 1931 in a flock of young chickens in the USA. Since that time, the disease has been identified in broilers, layers and breeders chickens throughout in the world. Vaccines to help reduce losses in chickens were first used in the 1950s.

Aetiology

Infectious bronchitis is caused by a coronavirus. It is an enveloped, single stranded RNA virus. Three virus specific proteins have identified; the spike (S) glycoprotein, the membrane or matrix (M) glycoprotein,  and nucleocapsid (N) protein (Figure 1). The crucial spike glycoprotein is comprised of two glycopolypeptides (S1 and S2). These spikes or peplomers can be seen projecting through the envelope on electron micrographs giving the virus its characteristic ‘corona’ (Figure 2). H1 and mos SN antibodies are directed against the S1 glycopolypeptide. The unique amino acid sequences, epitopes, on this glycoprotein determine serotype. The virus is fairly labile (fragile), being easily destroyed by disinfectants, sunlight, heat and other environmental factors. Infectious bronchitis virus has the ability to mutate or change its genetic make-up readily. As a result, numerous serotypes have been identified and have complicated efforts at control thorugh vaccination. Three common serotypes in North America are the Massachusetts, Connecticut, and Arkansas 99 IB viruses. In Europe, various ‘Holland variants’, usually designated using numbers (D-274, D-212), are recognised.

Several strains of infectious bronchitis have a strong affinity for the kidney (nephropathogenic strains). These strains may cause severe renal damage. This affinity for kidney tissue may have resulted from mutation as a result of selection pressure following widespread use of the modified live IB vaccines. That is, after prolonged use of live IB vaccines, which initially provided protection against IB virus infection in respiratory tissues, viral mutation allowed new tissues to be infected, where there was little protection. These viruses have become less prevalent in recent years.

Transmission

The IB virus is spread by the respiratory route in droplets expelled during coughing or sneexing by infected chickens. The spread of the disease trough a flock is very rapid. Transmission from farm to farm is related to movement of contaminated people, equipment, and vehicles. Following infection, chickens may remain carriers and shed the virus for several weeks. Egg transmission of the virus does not occur.

Clinical signs in young chicks

Clinical signs include coughing, sneezing, rales, nasal discharge and frothy exudate in the eyes. Affected chicks appear depressed and will tend to huddle near a heat source. In an affected flock, all birds will typically develop clinical signs within 36 to 48 hours. Clinical disease will normally last for 7 days. Mortality is usually low, unless complicated by other factors such as Mycoplasma gallisepticum, immunosuppression, poor air quality, etc.

Clinical signs in older chickens

Clinical signs of coughing, snezing and rales may be observe in older birds. A drop in egg production of 5-10% lasting for 10-14 days is commonly reported. However, if complicating factors are present, production drop may be as high as 50%. Egg produced following infection may have thin or irregular shells, and thin, watery albumen. Loss of pigment in brown-shelled eggs is common. In severe complicated cases, chickens may develop airsacculitis. Chickens that experienced a severe vaccination reaction following chick vaccination or field infection during the first two weeks of life may have permanent damage in the oviduct, resulting in hens with poor production.

Nephropathogenic stains have been recognised in laying flocks. These strains may cause an elevated mortality during the infection or long after as a result of kidney damage that progresses to urolithiasis. However, there are numerous causes of urolithiasis and it cannot be assumed that IB is the cause of this condition without supporting laboratory data.

Lesions

Lesions associated with IB include a mild to moderate inflammation of the upper respiratory tract. If complicating factors are present, arisacculitis and increased mortality may be noted, especially in younger chickens. Kidney damage may be significant following infection with nephropathogenic strains. Kidney of affected chickens will be pale and swollen. Urate deposits may be observed in the kidney tissue and the ureters, which may be occluded. Laying chickens may have yolk in the ovary may be flaccid. Infection of very young chicks may result in the development of cystic oviducts.

Diagnosis

Serologic testing to determine if a response to IB virus has occurred in a suspect flock is performed by comparing two sets of serum samples; one is collected at the onset of clinical disease and the second sample 3 ½ -4 weeks later. Serological procedures commonly used include ELISA, virus neutralisation, and Hl. Confirmation of IB requires isolation and identification of the virus. Typically, this is done in specific pathogen-free (SPF) chicken embryos at 9-11 days of incubation by the allcantoic sac route of inoculation. Tissues collected for virus isolation attempts from diseased chickens include trachea, lungs, air sacs, kidney, and caecal tonsils. If  samples are collected more than one week after infection, cecal tonsils and kidney are the preferred sites for recovery of IB virus. Virus typing has traditionally been performed by neutralisation using selected IB antisera. More recently, polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) have been used to differentiate IBV serotypes. Lesions in embryo are helpful in diagnosing IB, Affected embryos examined at 7 days after inoculation are stunted, have clubbed down, an excess of urates in the kidneys, and the amnion and allantois membranes are thickened and closely invest the embryo. These embryo will not hatch. IB field virus may have to be serally passed in embryos to adapt the field virus to the embryos before typical lesions are recognised.

Control

Prevention of infectious bronchitis is best achieved through an effective biosecurity programme. As a second line of defence, chickens in IB problem areas should be vaccinated with modified live vaccines to provide protection. The multiplicity of serotypes identified in the field presents a chalennge in designing an effective vaccination programme. To be successful in protecting chickens against challenge, it is essential to identify the prevalent serotypes in the region and to determine the cross-protective potential of available vaccines. In North America, the common sertypes used in most vaccinating programmes are the Massachusetts, Connecticut and Arkansas serotypes. These serotypes are available in both modified live vaccines and inactivated water-in-oil emulsions. Regionally important serotypes (e.g. California strains) may be included in inactivated vaccines. In Europe, various ‘Holland variants’ usually designated by number (e.g. D-274, D-1466) are recognised. Polyvalent vaccines, which contain multiple strains, are also available. Control of other respiratory disease, e.g. Newcastle disease, Mycoplasma gallisepticum, and strongly immunosuppressive disease, e.g. infectious bursal disease or Marek’s disease, must  not be forgotten.

Vaccines selection

IB vaccination programme is broilers involve the use of modified live vaccines. Vaccination of layers hgas historically involved administering a series of live vaccines and progressively increasing the aggresiveness of the route of vaccination, i.e. start with water administration and progress to fine particle spray, and strain of vacccine (highly attenuated to less attenuated). In breeders, a similar programme is often followed. However, prior to onset of production, an inactivated vaccine is also administered to stimulate antibody production. Inactivated vaccines stimulate higher levels if circulating antibodies than live vaccines and would be of value in a breeder programme where maternal antibody protection is neede. Modified live vaccines provide better stimulation of cell mediated (T cell system) and elicit a superior local antibody (immunoglobulin A, IgA) response as a result of local mucosal infection and thus would be of more value in protecting commercial layers.

With dozens of IBV strains having been identified around the world, choosing approriate strains for vaccination may seem a daunting task. The immue response produced to one strain, however, often shows a significant degree of cross-protection to heterologous challenge. Cross-protection has been demonstrated especially for the live type of vaccines. If the prevalent strains for a region have been identified, it is often possible to design a programme using commercially available vaccine strains Although no reasonable combination of IB vaccine strains provides full protection against all heterologous challenges, there are combination that offer broad coverage. Once the prevalent serotypes in an area have been identified, the use of modified live vaccines containing carefully chosen trains can be used to immunise broilers, layers and breeders. Additionally, polyvalent inactivated vaccines can be administered to breeders at point-og-lay. It has been demonstrated that ‘classical’ strains of IBV can act at least as partial primes for susequent administration of an inactivated infectious bronchitis vaccine containing variant dan standard strains. Inactivated IB vaccines do not stimulate local and cell=mediated immunity as effectively as modified live virus IB vaccines. However, they can provide a degree of immunity against variant strains without the risk of introducing new strain of IB into a poultry operation. Imprudent over-use of live IB vacines results in the vaccines becoming the problem rather than part of the solution.

While deciding which strains to utilise in an IB vaccination programme, the basic must not be ignored.  Good vaccination practise are especially important when administering live IB vaccines. It is relatively fragile virus and can easily be inactivated if proper vaccination procedures are not followed. Good practise include protection of the vacine from sunlight, removal of sanitiser from water used for mixing/administration and the use of a skim milk stabiliser.

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Necrotic enteritis – a silent profit robber

Figure 1

 A brief overview and a case report from india

Necrotic enteris (NE) was first described in chickens in 1961. NE is caused by the gram-positive bacterium, Clostridium perfringens. This article discusses a brief review of NE in the literature and a case report of NE in young commercial pullets in India.

Clostridium perfringens

It is an anaerobic bacterium, i.e. one that grows in the absence of oxygen, and it has the ability to form spores. The spores are small structures highly resistant to environmental stresses. They consist of a tough hard coat that encapsulates the bacterial genetic material and protein necessary for growth. By virtue of forming spores, the bacteria enter a dormant phase when environmental conditions are unfavourable and remain so for as long as necessary. Once present within a chicken house, clostridial spores can remain alive for centuries. Clostridia are capable of producing among the mos potent toxins ever known. It is the toxins that responsible for causing disease. They cause damage to the tissue and destroy red blood cells, thereby reducing the oxygen carrying capacity of the blood. In some cases, they prevent nerves from sending signals to the heart and lungs.

What is necrotic enteritis?

NE is a condition characterised by death or necrosis of the intestinal lining predominantly of the middle and lower small intestine which may be accompanied by necrosis in caeca and liver in some cases. It is transmitted with the ingestion of droppings contaminated soil, water, feed, or litter.

Figure 2

Triggering factors

In healthly chickens, clostridial bacteria normally live harmlessly in the lower gut and are found in the caeca and lower large intestine. The pH and high oxygen content of the healthy small intestine do not support growth of the organisms. For NE to occur, there needs to be a triggering factor that tips the balance in favour of the clostridial bacteria allowing them to proliferate and migrate to the upper small intestine.

Among the known trigger factor are:

• Direct damage to the intestinal lining by coccidial challenge or bacterial overgrowth.
• Feed factors that alter the gut environment like rapeseed, fishmeal, wheat or protein level.
• Immunosuppresion which reduces resistance to gut infections, e.g. CAV, IBD, Marek’s disease, physiological stress.
• Physical factors that damage the gut lining like litter material, a lack of grit or a change in physical feed presentation.

A Case report

In a commercial layer flock of 29 weeks, it was noticed that the peak production standard was no being maintained although morality was within an acceptable range. On investigation, it was foud that the birds were suffering from sub-clinical NE.

Figure 1 shows the changed appearance of the birds comb. Necropsy finding revealed enlarged gas-filled small intestine with the NE observed from the duodenum to the ileum (figure 2). The mucosal surface of the affected area of the intestine was covered with a tan orange pseudo-membrane. This “dirty turkish towel” appeareance is commonly associated with NE. Histopathological examination of the small intestine revealed extensive necrosis of the the villi and infiltration of the lamina proproa with mononuclear cells.

It was also observed that the flock was underweight and each bird was receiving only 207kcal metabolissable energy and 16.8g crude protein daily, compared to the requirements of 290kcal and 18g, respectively. Few birds were showing nasal dishcarge also indicative of mycoplasma infection.

Maize, de-oiled soybean meal, broken rice, sorghum, de-oiled peanut cake, fish and squilla were among the major ingredients of the feed.

The farm records indicated that the farmer had similar problems with previous flocks. For the treatment, it was recommendend that the feed formulation be modified to ensure the birds received adequate levels of energy, protein, lysine, methionine etc. Fishmeal and squilla were removed from the feed, which was supplemented with enzymes and tetramutin (combination of tiamulin and chlortetracycline).

Within 15 days, the flock showed good improvement with regards to the hen-day production, bodyweight etc.

-Dr. Avinash Dhawale,

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Nutritional modulation to enhance immunity in chickens

Prevention is better than cure, as they say. Many nutrients, energy, amino acids, vitamins and minerals - play different but significant roles in the immune response and so can contribute to keeping birds in good health, without the need for medication.

Presently, the aim of commercial poultry breeding is to achieve higher body weight and maximum egg production per unit of feed intake. However, there is a negative correlation between production and immunity in chickens as a result of the conflict between production and immunity, i.e. maturation and function oh the immune system. Accomodation of all the physiological demands within the limited resources, i.e. nutrients, available to birds may be the factor responsible for the negative relationship between performance traits and immunity. The genotypes with the maximum bodyweight exhibit lower immunity, as indicated by E. coli lesion score and cellular immunity antibody titres, compared to those having lower body weights. Therefore, the possibility of breakdown of the immune system in commercial chicken crosses is more evident nowadays than before.

In addition to genetic selection, certain non-genetic factors like dietary nutrient concentration also modulate the expression of the genes responsible for immuno-responsiveness by altering the maturity of the immune system and magnitude of antibody production.

Defence mechanism in chickens

Under intensive farming conditions, the poultry environtment contains ubiquitous micro-organisms that continuously challenge the bird;s immune system. Generally, the invading pathogen will be attacked by antibodies, whichs wil neyutralise, weaken and inactiveate the pathogen and finally, phagocytic cels will engulf the invader. The mechanism is quite effective in controlling extra-cellular phatogens, such as bacteria. For the intracellular pathogens-viruses-cell-medicated immunity (CMI) plays a key role. The CMI protects the host by destroying the cells that harbour the pathogen with the help of cytotoxic T-lymphocytes. Againts invading pathogens, the immune system produces a variety of compounds like acute phase protein (APP), proteolytic and hydrolytic enzymes, oxygen radicals and nitrogen derivatives, which destroy the invader or infective cells.

Nutrient recommendations are typically developed using indices of productivity such as growth, egg production and feed efficiency. The criteria for adequacy of immunocompetence are often ignored. Nutrients also influence the maturity of the immune system and magnitude of the antibody. During the acute phase of the immune response, the greatest nutritional need is for the synthesis and release of APP by the liver. The process requires more energy and amino acids than are normally needed for responding leucocytes. Interactions among various nutrients and imbalace or toxicity of nutrients lead to disturbances in normal physiology of the bird, with consequent immunosuppresiaon in chickens.

Energy

Variations on concentration of energy in the diet modulate the immune response in birds, probably due to the change in intake of nutrients, wich influence the immunity. Energy intake regulates the acitvity of the immune cells and activity of certain hormones, e.g. thyroxin, corticosteroids, growth hormones, glucagons, catecholamines, wich influence immunity. Variation in the level and composition of dietary fat also influence the immune response in chickens by altering the structure of the cell membrane and modulating the synthesis of prostaglandins. Mortality associated with E. coli and Mycobacterium tuberculosis was reduced by increasing the level of fat from 3% to 9% of the diet. Antibody titre against sheep red blood cells (SRBC) antigen was markedly increased with supplemental tallow at 6% in the chick diet. Higher levels of unsaturated fatty acids enhance immune function by stimulating macrophages.

Protein

The growth of bursa and thymus are relatively faster than the bird’s body growth. Therefore, it is important to supply the required quantity of protein, particularly during the early growth phase. Deficiency of protein at this stage leads to the improper development of lymphoid organs. Several research workers have suggested that there is a higher amino acid requirement for immunity than for growth. However, the influence of level of protein in diet on severity of disease depends on the type of infective organism. The lesion score to E. coli  inoculation dcreased with the increase in the protein level (18, 20.5 and 23%) in broiler diets. With coccidiosis, the mortality decreased from 32% to 8% in chickens fed protein-deficient diets compared to those fed a normal protein level.

High dietary protein increases the activity of trypsin in the chicken gut. A high level of trypsin in the gut leads to a faster release of coccidia from oocysts, which will aggravate the disease symptoms.

Dieatary methionine levels in exces of those required for maximum growth are essential for maximising immunity. Methionine is required by the thymus-derived- T-cell function. Methionine deficiency produces severe lymphocyte depletion and atrhopy of the bursa and an increased suspectibility to Newcastle disease coccidiosis.

Cystine supplementation also stimulates cellular and humoral immunity (70 to 84% as effective as methionine)

Deficiency (16 to 50%) of branched-chain amino acids, i.e. isoleucine, leucine, and valine, reduces the antibody titres againts SRBC in broilers.

Immunoglobulins contain a high concentration of valine and threonine. A deficiency of either of these amino acids reduces the immune response in chickens. A higher ratio between leucine to valine + isoleucine reduces immunity due to structural antagonism between the three amino acids. The absorption of valine and isoleucine are inhibited by a high leucine content din the diet.

Increasing the dietary concentration of lysine improved the haemagglutination and agglutinin titres, and IgG and IgM levels.

Arginine is a substrate in the synthesis of nitric oxide, a cytotoxic product that is helpfu in phagcytic activity of macrophages and kills bacteria and intracelluar parasites.

Vitamins

Vitamins act as co-factors in several metabolic functions in immune reactions and therefore, deficiencies  of vitamins cause impairmentt of immunity. Generally, higher levels of vitamins than the current recommendations will increase the immune response.

Retinal

This vitamins Is important for maintaining the cellularity of the lymphoid organs and epithelial tissues and for enhancing both cellular and humoral immunity. Vitamin A helps in maintaining the mucous membrane of natural orifices in healthy condition to prevent the invasion of microorganisms. Vitamin A directs differentiation and development of B-lymphocytes. The concentration of vitamin A in the diet modulates the expression of retinoic acid receptors on lymphocytes in chickens.

The production of immunosuppressive agents (hydrocortisones) is reduced with higher levels of vitamin A in the diet. Furthermore, deficiency of vitamin A causes keratinisation of basal cells of the bursa and impairment on the response of T-lymphocytes. Therefore, deficiency of vitamin A impairs immunity by producing defective T, B-lymphocytes, impaired phagocytosis and reduced resistance to infection. Increased morbidity due to Newcastle disease virus has been reported due to a deficiency of vitamin A in the diet. The requirement of vitamin A for maximum immunity, i.e. lymphoid organ weight, was higher than for the bodyweight gain in the chicken. An increase in vitamin A from 12850IU to 42850 or 74045IU/kg decreased mortality due to E. coli, and CRD in chickens and increased the rate of clearance of the pathogen from the blood. However, the benficial effect of higher levels of vitamin A depends on the concentration of other fat-soluble vitamins in the diet. An excessive level of vitamin A interferes with the utilisation of vitamins D and E.

The administration of 60IU of vitamin A per chick per day during a severe attack of coccidiosis reduced mortality from 100% to almost zero. However, practical chick and young layer diets should contain 4000 and 2000UI/kg, respectively. To minimize stress damage and also to prevent immune suppresion, dietary vitamin A levels shoul be increased to ten tomes the normal requirement. A combination of vitamin A (14000IU/kg) and zinc (65mg/kg) has been shown to enhance growth and both humoral and CMI immunity in chickens.

TO BE CONTINUE……

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Are American Commercially Produced Eggs Safe from Avian Influenza?

Why American commercially produced eggs are safe to eat:

When chickens become sick with Avian Influenza, one of the first signs of illness is that they stop laying eggs. In High Pathogenic Avian Influenza (HPAI), the more severe form of the virus, the illness is very sudden, egg production stops, and many of the birds will die from the disease. 

In the United States, if HPAI should be identified within an American commercial flock, at the first sign of illness the farm would immediately be quarantined. If eggs are laid after the onset of illness (at most one or two eggs per hen) the eggs would most likely be of inferior quality and would not make it through the washing, grading and inspection process. The eggs would not even be sent to the packing plant since the farm would be under quarantine.

How do we know that cooking eggs thoroughly will inactivate the virus?

In an effort to confirm that pasteurized egg products are safe, researchers at the USDA Southeast Poultry Research Laboratory (Swayne, Avian Pathology, 33(5), 512-518) artificially put avian influenza virus into egg products and treated the sample with typical pasteurization processes. The temperatures during pasteurization and cooking of eggs and egg products were found to be more than adequate to inactivate any virus particles. This further ensures that eggs and poultry meat are safe when handled and cooked properly.

How is the American commercial egg supply different from other
countries and how are American consumers protected?

A key difference between the countries in Asia which have been severely affected by this outbreak, and here in the US, are our production practices and confinement of poultry. Most consumers in the US have no contact with live poultry of any kind. In Asia, the practices are very different and poultry are free to roam villages. The isolation of poultry production, the enhanced biosecurity procedures, and the lack of contact with live poultry, are all practices that will protect the US from experiencing the same kind of outbreak of AI that we have seen in Asian countries. In addition, our American poultry processing, inspection, and distribution systems are designed to detect any problems immediately so that the affected products never reach US consumers. Commercial eggs are safe to eat and consumers should have no concerns about continuing to enjoy properly cooked eggs.

www.eggsafety.org

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Bird Flu

All domesticated poultry species are susceptible to Avian Influenza (AI). Also called avian flu or bird flu called. In the outbreak in 2003 of the H7N2 type that appeared on a limited scale backyard poultry had become infected. Research showed that the risk of infection and spread of the virus in backyard poultry is much smaller than commercial poultry. (1)

Backyard poultry vaccination against bird flu

At the time of the outbreak in 2003 was a ban on vaccination. Due to the worldwide spread of the dangerous H5N1 virus to humans, this vaccine ban on the initiative of the Dutch government in 2006 eased. Hobby poultry should be vaccinated against bird flu since then. The Dutch government must get permission before applications''Brussels''. This permission is for a specified period issued.

The protocol for preventive vaccination was initially - two blood tests, export ban on backyard poultry vaccinated, vaccination at home - has changed since 2007. The blood test is not required before and after vaccination is not mandatory for all hobby keepers blood sample. This will happen randomly. Vaccinated animals may be transported to another Member State provided that State do not object. (2)

The Dutch government since 2006 makes a distinction between commercial poultry and backyard poultry in terms of screening / confinement. In a low risk of infection may backyard poultry, except waterfowl, roam freely. Vaccinated hobby poultry is also at high risk exempt from the screening requirement. (3) All types of vaccines against avian influenza H5 and H7 that since 2007 the European Union on the market, meet the quality standards and are safe and effective use (4).

ResearchSince the outbreaks of bird flu found on businesses regulated research (monitoring) site. Also, wild birds are tested for the presence of bird flu. Worldwide there is much scientific research. It is under further revealed that the H5N1 virus can survive long outside of birds. Varies depending on the circumstances the survival of two weeks to two months. The colder and drier air, the longer the virus remains alive.

It is also clear now why it is that ducks are carrying the virus, not ill. U.S. scientists have discovered a gene that causes bird flu infection with duck a problem through. Chickens do not have this gene.

Low Pathogenic and High Pathogenic

With bird flu a distinction between low pathogenic and highly pathogenic virus. The low pathogenic virus is not very ill, the highly pathogenic is very sickening. For the low pathogenic virus is a different approach than for the highly pathogenic virus. In an outbreak of low pathogenic virus is only removed the infected farm, an outbreak of highly pathogenic virus are also businesses in the area cleared. Vaccination of companies is possible, but for economic reasons still not fully accepted. Also, the existing vaccine is not fast enough to operate a poultry outbreak in a highly dense area quickly to control (see appendix Control of Highly pathogenic Influenza Avia)

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Newcastle Diseases

Newcastle disease and New Castle Disease (NCD) is caused by the virus of the Paramyxoviridae family, genus Rubulavirus. Newcastle disease is endemic in many countries.The incubation period for Newcastle disease is four to six days. The symptoms are wheezing, coughing, hanging from the wings, turning the head, paralysis, decreased egg production, distorted egg, greenish, watery diarrhea, swelling around the eyes and the neck. Mortality depends on the type of poultry and the virus type.
Newcastle disease virus may be present in almost all birds, both domesticated and wild birds. Directly susceptible to the virus are chickens, turkeys, quails, pigeons, ostriches, parrots and canaries species. Other birds are less sensitive and exhibit milder symptoms. Less sensitive species can carry and excrete virus without showing symptoms.
The transmission of the virus takes place including the feces of infected animals. The man can play a role in the transmission. There is no treatment. (1)
SpreadDistribution of the New Castle Disease and Newcastle disease within a flock is through inhalation of virus or the absorption of water and / or food contaminated by manure or secretions of loft mates.Spread from an infected flock to a sensitive torque is available over the air, contaminated water droplets and particles through mechanical vectors. Clothing, footwear of visitors, crates, containers and egg trays are the most important.Other distribution vectors include other animals, including flies, litter and contaminated poultry products (meat and eggs).Spread of virus from a reservoir of wild birds may be in direct contact with infected wild birds and poultry business. Infection is possible if infected wild birds in the immediate vicinity of the barn and stop conditions for distribution via the winds are favorable. In this context also (post) pigeons a potential source of infection.
VaccinationFor Newcastle disease and Newcastle disease vaccination is a requirement for commercial farmers, hobby farmers with their animals to shows, and holders of pigeons participating in races. Several vaccines are freely available. This compulsory vaccination must be performed by a veterinarian.In addition, owners themselves voluntarily vaccinate their animals. The vaccination should be carefully conducted. The oogdruppelmethode is the best, then spray-inoculation, and finally the drinking water vaccination. Experienced bird keepers, the vaccination itself can perform well. Follow the instructions of the veterinarian well. Not every vet has the vaccine in stock but can order or at a poultry veterinarian involved. It is very useful vaccination after 14 days to repeat. The animals build a good resistance.
Under the control scenario are sick animals euthanized and non-diseased animals are kept indoors 60 days and checked for disease. After 30 and 60 days, these animals by the FDA sampled for NCD and then vaccinated. Is a location free from disease, it will be released after 60 days.
In pigeons is a variant of Newcastle disease found that in sudden death without obvious abnormalities lead. It is the pigeon paramyxovirus-1. This virus would in due course be transferred to chickens, where it could develop into a malignant variant. In couples who have a good protection against Newcastle disease virus, this little birds can do damage.

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Gumboro

Gumboro Disease, also known as Infectious bursitis of Infectious Disease Scholarship (IBD) called, is caused by the Gumboro virus. The disease can be clinical or subclinical course and caused much damage in both cases.
SymptomsA couple has affected general illness with a watery, slimy stools white (by uraatbijmenging). In a torque-sensitive, the whole flock suddenly attacked and lead to death. Although the literature indicates that clinical (visible) infections are not common in animals less than three weeks, we see in practice, often at an earlier stage clinical infections. The earliest infection was determined at the age of 9 days.
CauseThe disease is caused by the Gumborovirus, also known as Infectious Disease Scholarship virus (IBD) called. Natural infection occurs by uptake of the virus through the beak / mouth (oral route). The virus was 5 hours after infection to demonstrate in cells of the small intestine and liver. A strong virus replication occurs in the bursa of Fabricius from 11 hours after infection. The main host for the IBD virus (IBDV) is the chicken, continue his regular natural infections in turkeys and ducks. For pheasants and ostriches, the IBD virus is isolated, quail may also be sensitive. The disease occurs worldwide.
IBD has two serotypes: serotype 1 and serotype is the most important causes disease in chickens, serotype 2 is found in chicken, turkey and duck, but is not pathogenic. Within the serotype 1, the so-called variant IBD viruses' for. These cause many problems in the USA. Within a serotype, a further subdivision into groups as possible. This is done based on differences in amino acid sequence. The groups with modern DNA techniques to map. The virus has an incubation period of 2 to 3 days.
Infection RouteVirus Spread within a flock is through direct and indirect contact. The manure is the main source of dust stain. Infected animals secreted up to two weeks after infection with the virus much manure. Transmission through the air (aero gene transmission) plays no role. There is no evidence of transmission through hatching (vertical transmission). Also, we do not know 'carriers'.The virus is highly resistant, thus IBD problem once infected premises may remain long. After removal of an IBD-infected flocks remains the loft for at least 122 days infectious, water, feed and manure samples from a contaminated pen after 52 days still infectious. IBD virus includes sensitive to chloramine disinfection with 2% (Halamid), formalin and glutaraldehyde.
Between companiesSpread to other firms takes place through people, animals or contaminated materials. Because of the resistant nature of the indirect transfer easily find Gumborovirus place. Wild birds, rodents and polystyrene beetles can transmit the virus to other couples and / or companies. The virus can survive for long in manure. Contaminated manure near businesses is a clear risk factor.

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Avian influenza

Avian Influenza

(also known as bird flu, avian influenza) is a form of influenza virus that is hosted by birds causes, but may infect several species of mammals. It was first recognized in Italy in the early 1900s and is now known that the whole world. A strain of the H5N1 type of avian flu virus, which was created in 1997, when the most likely source identified for a future pandemic.

Strains of avian influenza can infect virus different types of animals, including birds, pigs, horses, seals, whales and humans. However, spreading wild fowl act as natural asymptomatic carriers, they are prone to domestic shares. Bird flu virus spreads in the air and in manure and there is no evidence that the virus can survive in well cooked meat.

Diagnosis

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How to recognize bird flu
What should you should

       * Ruffled feathers
       * Soft-shelled eggs
       * Depression and droopiness
       Sudden drop in egg production
       * Loss of appetite
       * Cyanosis (purplish-blue coloring) of wattles and comb
       * Edema and swelling of the head, eyelids, comb, wattles and hocks
       * Green Diarrhea
       * Bloody nasal
       * Co-ordination problems, including loss of ability to walk or stand, and
       * Pin-point hemorrhages (most easily seen on the feet and calves)
       * Shortness of breath
       * Increased death losses in a herd
       * Sudden Death
       * nasal discharge

  
Poultry Vaccination as a strategy for controlling AI in commercial birds

Outbreaks of avian influenza in the poultry industry cause devastating economic losses and is generally controlled through extensive culling of infected birds. Alternative strategies also use vaccination as a supplementary control measure during avian influenza outbreaks.

Advantages of Vaccination

• Vaccination reduces susceptibility to infection.
• A higher dose of virus is necessary to infect the vaccinated birds.
• Vaccinated birds shed less virus.
  - Decreased contamination of the environment.
  - Decreased risk of human infection
• Used strategically vaccination compliments a stamping out strategy by slowing/stopping the spread of the virus

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