Friday, October 30, 2015

Gangrenous dermatitis: a ‘gut disease’?

Gangrenous dermatitis (GD) is a bacterial disease of chickens and turkeys which primarily affects the skin and tissues below the skin in the abdomen of the bird. Gangrenous dermatitis is bilieved to be caused by species of clostridia, usually Clostridium perfringens or Cl. Septicum,  but many other bacteria have been isolated from Gangrenous dermatitis lesions.

Dr Donald Ritter, director of health services, Mountaire Farms, Inc, speaking at Delmarva Poultry Industry National Meeting, said that the number of flock affected by Gangrenous dermatitis in commercial poultry has been on the rise in the USA in recent years.
Gangrenous dermatitis occurs in poultry flocks raised on built-up litter. Dr Ritter said that historically, this condition has been linked to flocks whose immune systems were impaired by prior infection with infectious bursal disease virus or with chicken anaemia virus, but that many flocks with Gangrenous dermatitis today appear to have protection against these viruses.

Broiler flocks with Gangrenous dermatitis experience a sudden increase in mortality at 5-7 week of age – up to 1% daily for up to 2 weeks. Turkey flocks experience a similar mortality pattern but from 12-20 weeks of age. It is rare to find birds with Gangrenous dermatitis lesions alive.

Clostridia are spore-forming and so they can persist in the environment for long periods of time and are resistant to most disinfection procedures. Once affected by Gangrenous dermatitis, many houses envolve into endemic Gangrenous dermatitis sites where the disease recurs in most flocks. There is also a seasonal pattern observed in the incidence of Gangrenous dermatitis cases in chicken: the greatest number of cases occurs during spring and summer. Penicilin is the treatment of choice.

Gangrenous dermatitis skin lesions consist of dark purple areas with excessive red thickened serous exudate (‘jelly’) with associated emphysema (‘gas’) in subcutaneous tissue around the hips, abdomen and occasionally the wings in chickens. Typical skin lesions are located in the tail head area of turkeys. Some lesions are close to skin scratches in de-feathered hip areas.

Because Gangrenous dermatitis lesions are often found close to damaged areas of skin caused by toe-nail scratches, the presumed route of infection has been through the damage skin. The localised skin infection then produces bacterial toxins that quickly kill the bird. However, many birds with Gangrenous dermatitis lesions have intact skin in affected areas, or may have lesions on the wings or crop areas of the bird also unaffected by skin damage.

Clostridia form part of the normal anaerobic intestinal flora of poultry, so the itestine provides another possible direct route of infection. The bacteria may enter the bloodstream via mucosal disruption in the gut. Damage to the gut caused by coccidia has been proposed as a source of Gangrenous dermatitis infection.

 Dr Ritter conclude, “I believe that Gangrenous dermatitis will be proven to be primary ‘gut disease’ when all field and research data have been collected and carefully scrutinised. (Watt publishing)
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Another good reason to control houseflies: they carry bird ‘flu virus’


Avian influenza has taken a great toll on the human population and on the poultry industry over much of the world. One aspect that has occupied scientist is the possible method of transmission, of which there appear to be many. Wild birds have received much oh the attention until now but studies shows that flies can be virus carriers too (Dr Terry Mabbett)

Poultry farms and houseflies need no introduction. Universal infestation by Musca spp. and close relatives is part and parcel of livestock production, especially in hot climates. Musca domestica (common houseply) is a dipterous insect of cosmopolitan distribution and versatile within its environment, feeding and breeding on all kinds of organic matter including food and animal feed, garbage, faeces, sewage and animal carcasses.
Houseflies constantly move between ‘dirty’ areas of putrefaction teeming with pathogens and ‘clean’ areas including feed storage and animal housing. As such they are a major source of disease and implicated in the transmission of over 30 different diseases caused by bacterial, protozoan and virus parasites.

Adult flies carry disease

Houseflies breeding in media brimming with bacteria, including pathogens, might be expected to convey at least some from the larval (maggot) stage to the adult fly emerging from the pupa case. But early research showed the hostile chemical nature of the larva gut and antagonism by gut microflora maintained a generally low level of pathogens. More than one-fifth of houseflies and almost tow-fifth of green bottle blowflies (Lucilia spp) were sterile on emergence.

The main risk of disease spread is from adult houseflies contaminated with bacteria, protozoa and virus particles. Houseflies could theoritically transmit pathogens on their feet but opportunities for attachment to such small surface areas are considered tiny and microbes are susceptible to dessccation.
Hazards are focused on housefly feeding, sucking up liquid from putrefying food and faeces supporting high concentrations of pathogens. Transmission via vomit drops presents risks, but adult houseflies vomit originates from sugary fluids stored in the crop and presents a correspondingly lower risk than excretory deposits. Research which showed Salmonella typhimurium multiplying in the mid-and hind-gut and passing out intermittenly over an interval of at least one week lent huge weight to these arguments.
Houseflies are well established vectors of food poisoning bacteria like Salmonella spp. and Eschericia coli harboured by birds. More recently, transmission of poultry virus diseases like Newcastle disease and avian influenza (AI) by houseflies is considered, in addition to spread by direct contact by contaminated faeces and bird secretions.

Houseflies carry virus disease particles

Recent research at North Carolina State University has shed new light on the role of Musca domestica in the potential transmission of Newcastle disease virus (NDV). Adult flies carried an infectious dose in the gut for three hours after feeding and researchers Drs Wes Dawson and James Guy considered this might be important for spread of the virus when fly populations are high and in contact with highly virulent velogenic NDV strains.

Newcastle disease virus is dedicated disease of poultry but AI is now under the spotlight because the H5N1 highly pathogenic strain is a zoonosis transmitted to human from animal. The march of H5N1 has been far and fast leaving precious little time to study infection and spread in detail. H5N1 virus spread by wild birds is a relatively recent focus since the Qinghai strain H5N1 appeared in wild fowl in western China during may 2005 and subsequently sped all the way to Western Europe and West Africa in just six month.
There are several reported instances going back 20 years of houseflies carrying the AI virus and suspected as a mode of transmission. In 2005, they were highlighted and summarised by scientists from Novartis Animal Health as part of an article reinforcing the importance of good fly control on poultry farm.
Following reports in 1985 of houseflies in poultry houses contaminated with AI, a detailed study was presented at a conference in Australia in the following year. The study was based on a serious 1983/4 outbreak of H5N2 in Lacaster Country, Pennsylvania, USA. Up to 90% of affected flocks died and various modes of transmission, including direct contact between birds, mechanical vectors and vector insects and especially houseflies, were considered.

Fifteen different insect species-mainly flies and beetles- were collected in 300+ species-specific samples, each containing 10-60 insects. More than one-third of the adult Musca Domestica samples contained AI virus particles, as did one-third of samples comprising less abundant fly species like Ophyra (dump flies) and Coproica (dung flies).
During the 2004 H5N1 outbreak, Asian scientists identified the virus in blowflies caught near a poultry farm in Kyoto in western Japan, which had experienced a disease outbreak in the preceding months.

Parallels with West Nile virus

If the AI virus is present in Musca Domestica or other flies, it does not necessarily mean transmission to poultry, let alone extra risk of human infection. However, the possibility of spread by flies does open a whole new dimension on this virus disease. A comparison can be drawn with West Nile virus (WNV), a flavivirus causing disease in wild birds, horses and humans and transmitted amongst theese three groups by the blood-sucking activity of mosquitoes, mainly Culex spp

West Nile virus is a zoonosis and an arbovirus, a virus particle transmitted by an arthropod animal such as an insect, mite or tick. This efficient means of West Nile virus transmission between humans, wild birds and horses by airborne blood-sucking insects has facilitated a breathtaking speed of spread. From a single case in the West Nile region of Uganda in 1973, the virus now threatens many parts of the world and spread right across North America from New York to California in just three years (1999 – 2002).
That the AI virus can be spread by winged insects as well as wild birds underlines the need for efficient fly control on poultry farm, along with other stric biosecurity measures.
Dr. Terry Mabbet, Potters Bar
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Thursday, October 29, 2015

Testing a probiotic mixture for broiler chickens

Report of a trial in Bulgaria testing the effects of a mixture of probiotics, yeast and organic on the growth and gut health of broilers. The experimental mixture resulted in a shift in the microbial balance in the gastrointestinal tract in favour of Gram-positive bacteria. There were also significant emprovements in both final weight and feed conversion

It is known that the disorder in the compostion of normal gastrointestinal microflora in animals can lead to excessive proliferation of E. coli and coliform baceria, followed by various pathoglogies. A diet of skim milk powder, soybean meal or fishmeal has high acid binding or buffer capacity. This attribute, together with high intestinal pH, allows pathogenic Gram-negative bacteria such as E.coli and coliform bacteria to colonise the digestive tract causing inflammation and digestive disorders, so the gut absorbs fewer nutrients.

Balancing the gut microflora

In stressed birds, the number of E.coli in the gastrointestinal tract increases together with intestinal pH, thus decreasing Gram-positive microflora and producing dysbacteriosis of Gram-negative pathogenic bacteria that colonise intestines, cause inflammation of intestinal mucosa, decreasing the absorption of nutrients and stunting the growth of birds.
In some instance, the continuous administration of high doses of antibiotics or the use of sub-therapeutics or the use of sub-therapeutic doses of antibiotics was followed by dysbacteriosis and infection with Proteus, Pseudomonas and Aspergillus spp. As well as Candida albicans and other pathogens. A level of E.coli  of more than 300.000/m3 air causes microbial stress and may lead to an outbreak of colibacillosis in chickens.
In recent years, numerous studies have been carried out, with the aims of normalising the intestinal microflora composition and preventing the animal’s gastrointestinal tract from being colonised by pathogenic organisms. The activities of Lactobacillus bugaricus and Streptococcus thermophilus  were found to inhibit enteropathogenic E.coli in vitro. It is sometimes recommended to supplement poultry feeds with lactic acid, bacteria and yeast at times of stress. Some data has demonstrated that an acid environment (pH 3.5-4.0) favours the development of lactobacilli and inbibits the replication of E.coli, salmonella and other Gram-negavite bacteria known to cause gastrointestinal diseases. Acidic additives are especially useful for young animals because they reduce the Gram-negative bacteria and increase the Gram-positive organisms, leading to improvements in the health and weight gain of the animal. A combination of organic acids and probiotics has had synergistic influences on these two parameters in broiler chickens.

Previous work in Bulgaria

We have found out that lactic acid bacteria (L. bulgaricus) and Str. Thermophilus inhibited E.coli, S. enteritidis, St. aureus and Listeria monocytogenes. The inhibitory effect was measured by the diameter of the sterile zone around the well containing the probiotic. The suspension experiment revealed that this probiotic inhibited the count of the aforementioned pathogens by up to 99% in combined vultivation. All this is important for the colonisation of the gut with pathogenic micro-organisms and their adherence to intestinal mucosa epithelium.
The results of our studies showed 4% citric acid and 4% tartaric acid inhibited the growth of several Gram-negative bacteria such as E.coli, Proteus spp, Pseudomonas spp, S, entiridis and some Gram-positive organisms like L. monocytogenes and St. aureus. These organic acids reduce considerably the contamination of litter with such organisms and simultaneously, neutralise ammonia production. At the same time, the balance between Gram-positive and Gram-negative micro-organisms is optimised and the risks of re-infection and microflora imbalance are diminished.
The data from our experiments showed a huge inhibiroty effect over the 90% on the E. coli count in the feed. The highest effect recorded was more than 99% in the probe with the probiotic mixture, which was though to be due to a synergism between the active componenst. There was a correlation between this effect and a lo pH.

The latest study

The trial, with a total of 60 birds, showed that Gram-positive bacteria accounted for only 10% of the microbial microflora, while Gram-negative organisms made up 90% of the microflora in the control group of broilers. In the experimental group, treated with probiotic (3% lactic bacteria plus 1% bakers yeast) plus organic acid (0.7% citric acid) in the feed troughout the growing period, Gram-positive bacteria predominated (77-80%). The control birds had between 3 and 5 times more E. coli per gram of colon that the experimental birds at 20 and 42 days of age. They also had a coliform count at 20 days that was more than six times that of the treated birds and a yeast count of between 12 and 250 times higher than the birds receiving the combined probiotic mixture.

In conlclusion

The maintenance of an optimal balance between Gram-positive (77-80%) and Gram-Negative (20-33%) microflora in the avian gastrointestinal tract as well as good health and performance can be achieved in broilers with a combination of probiotics, yeast and organic acids in the feed.
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Wednesday, September 23, 2015

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.


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.


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.


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.


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 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.


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.


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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Monday, September 14, 2015

Beat fowl pox with pigeon pox

Fowl pox is an economically important disease of poultry because it leads to a drop in egg production and to mortality. Fowl pox is a slowly spreading disease characterised by the development of:
  • -          Discrete nodular proliferative skin lesions on the non-feathered parts of the body (cutaneous form) or
  • -          Fibrino-cerotic and proliferative lesions in the mucous membrane of the upper presiratory tract, mouth and oesophagus (diptheric form).
The incubation period for the naturally occuring disease varies from 4 to 10 days in chicken.


Because of its genetic make up and inherent stability, fowl pox virus (FPV) can persist in the poultry house and become a source of infection for suspectible future flocks. The increased frequency of the disease is perhaps due to the closer confinement of chickens, especially in multiple-age complexes. Such conditions provide opportunities for the transmission of disease directly from bird to bird as well as in the air. High poultry densities and dirty house increase the chances of spreading the disease.

Types of vaccines

Live virus vaccines are used for the immunisation of birds against fowl pox. These contain a minimum concentration of 10 EID/ml to establish a satisfactory take and good immunity,
Fowl pox and pigeon pox virus vaccines labelled ‘chick embryo origin’ are prepared from chorio-allantoic membrane. Fowl pox virus vaccine labelled ‘tissue culture origin’ is prepared frominfected chicken embryo fibroblas culture. If fowl pox appears in a flock in an initial outbreak and only a few birds are affected, the remaining birds should be vaccinated.
The ‘chick embryo origin’ vaccine contains live fowl pox virus capable of producing serious disease in a flock if it used incorrectly.
Fowl pox virus vaccine is commonly applied by the wing web method to 4 week old chickens and to pullets about 1-2 months before the expected onset of lay. This vaccine must not be used for hens already laying.
Attenuated fowl pox virus vaccines of cell culture origin can be used effectively on chicks as young as day-old, sometime in combination with Marek’s disease vaccine.
Pigeon pox vaccine contains live, non-attenuated, naturally occuring virus form pigeon. The virus is less pathogenic for chickens. The vaccine may be applied by the wing web method and can be used in chickens of any age. It is usually administered to chicks at 4 weeks of age or about one month before the onset lay.

A case study

On a breeder farm, severe fowl pox occurred in a flock of grower at 6 weeks of age. The birds had not been vaccinated and so the infection spread rapidly through the flock. The lesions were mainly on the non-feathered parts of the legs and there were a few cases on the face. Though there was no mortality, the disease disturbed the scheduled operation for the flock. Virucidal spray, antibiotics and additional vitamins were measures taken to control the outbreak and within 6 weeks, almost all the birds recovered with desquamation of the scales of the lesions (Figure 1, 2 and 3)
For the next flock, pigeon pox vaccine was used subcutaneously at 18 day of age. Only 9 days later, the first sign of pox were noticed, with lesions similar to the previous batch. Clearly, the birds were in the incubation period when the pigeon pox vaccine was administered. For the next flock, the pigeon pox vaccine was given on day 13. Symptoms of fowl pox were observed, but not until week 5 and only in a mild form. It should be noted that the growing birds were raised adjacent to a layer operation. The layers were vaccinated against fowl pox in weeks 7 and 13.
From this study, it appears that pigeon pox vaccine offers potential as a tool for the control of fowl pox.
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Wednesday, September 9, 2015

Necrotic enteritis – a silent profit robber

comb necrotic enteritis
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.

necrotic enteritis
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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Monday, September 7, 2015

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.


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.


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 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.
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.

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Saturday, September 5, 2015

Avian Influenza: Human Pandemic Concerns



The likelihood that the next human influenza pandemic virus will emerge from the Asian strain of the H5N1 high pathogenic bird influenza virus that is causing widespread outbreaks in Eurasia remains unknown. (See Glossary for italicized terms.) Because these bird influenza outbreaks remain primarily an animal disease, there is hope that a human pandemic can be prevented. Eradication of the H5N1 high pathogenic bird influenza virus needs to occur at the farm level in the countries where it is currently circulating. Funding of prevention, surveillance, and eradication efforts in the countries where outbreaks are occurring or in at-risk countries will provide tools needed to facilitate the eradication process of this virus where it is detected and will prevent further spread and subsequent economic loss. Most importantly, stopping the spread of this virus
will decrease the opportunity for the virus to emerge as the next human pandemic influenza virus. Every new poultry infection, and subsequent human exposure, gives the virus an opportunity to adapt directly to humans or to exchange genetic material with other influenza viruses, including human influenza subtypes; either event increases the chances that the bird influenza will become a significant human disease.


A pandemic is an occurrence of a disease in excess of its anticipated frequency that is geographically widespread (perhaps globally). Essentially, a pandemic is an epidemic with a much broader geographic distribution. Pandemics occur when human populations are exposed to highly transmissible disease organisms to which they have little or no immunity. This exposure can result in infections, which result in disease. The organism then escapes the infected human and is transmitted to the next susceptible human. Because the human population is immunologically naïve, every person exposed to the organism is potentially susceptible and may become infected. This process can result in rapid spread of the disease within a population and subsequent spread to distant populations. Pandemics generally spread worldwide within 1 to 3 years. As long as susceptible humans continue to come into contact with the infectious organism, the disease continues to spread. This cycle stops only when large portions of the population become immune to the infection and are no longer shedding the organism in large numbers. Immunity occurs when people become infected, recover from the disease, and have circulating antibodies to protect them from future disease.

Influenza A Viruses

Influenza viruses are identified by proteins that are unique to their virus “type” and “subtype.” The type designation comes from two internal proteins, known as the nucleoprotein and matrix proteins and includes the type A, B, and C influenza viruses. Type A influenza viruses are the most common, and infections have been reported in mammals such as swine, horses, cats, dogs, marine mammals, mink, and humans, as well as in birds. Influenza A viruses have caused several pandemics in humans throughout history; type B and C influenza viruses also commonly cause human disease, but disease outbreaks generally are limited in size. Influenza A viruses are characterized further according to the antigenic characteristics of two surface proteins known as hemagglutinin (H) and neuraminidase (N), resulting in a subtype designation. There are 16 H subtypes and 9 N subtypes currently identified, resulting in 144 different possible combinations of H and N subtypes among the influenza A viruses. The unique segmented structure of the genetic material in influenza A viruses makes them inherently unstable and subject to genetic change (Swayne and Halvorson 2003). 
Humans are commonly infected with H1, H2, and H3 subtypes of influenza A viruses. Viruses of the H5 and H7 subtype are of the most concern to agriculture because some strains have historically caused severe disease in poultry. Because most influenza A viruses are relatively host specific, human influenza viruses generally do not infect birds and bird viruses generally do not infect humans. Certain influenza A viruses, however, have exhibited an unusual ability to infect more than one host species. When influenza A viruses from two host species co-infect the same animal, the viruses have the opportunity to exchange genetic  material that codes for the internal and surface proteins, a process known as antigenic shift. This exchange could result in an emerging virus with a new or expanded host range. As a result, the new virus could infect host species that have never been susceptible before and also could cause a change in the ability of the virus to cause severe illness (Perdue and Swayne 2005). This type of change in a virus capable of spreading among humans could produce a pandemic. Although some pathogenic organisms remain unchanged for many years and can be controlled with vaccines that protect the recipient for a lifetime, influenza A vaccines do not fit into this category. The influenza A viruses accumulate point mutations resulting in sequential minor changes in the dominant circulating strains. This process is known as antigenic drift. Therefore, the influenza vaccine is evaluated yearly and changed frequently to protect against new and emerging strains of influenza A viruses. This is why people in high-risk groups are encouraged to be vaccinated with updated influenza A vaccines every year. 
The subtle changes seen from year to year in influenza viruses generally do not lead to widespread severe disease, but they do make it unfeasible to stockpile large quantities of vaccine for periods longer than 1 to 2 years. Subtle changes in influenza viruses can render vaccines less effective with time. Sudden major changes can render vaccines totally ineffective. 

Historical Pandemics

There were three influenza A pandemics in the twentieth century. The influenza pandemic of 1918 was the deadliest. This pandemic may have began in the United States as an epidemic that was confined largely to military bases and prisons. Public health officials were not overly concerned with the disease because infections tend to spread rapidly among people living in crowded conditions. When American troops took the virus to Europe during World War I, it quickly became established in Europe and spread to Russia, North Africa, India, China, Japan, the Philippines, Brazil, and New Zealand. American troops returning home brought the virus back to the United States and it spread into the civilian population. Almost 700,000 people died from influenza in the United States alone, and 20 to 50 million people died worldwide. Two additional influenza A pandemics have occurred since 1918: the “Asian flu” that resulted in one to two million
deaths in 1957–58, and the “Hong Kong flu” that resulted in approximately one million deaths in 1968–69 (Carver 2005). Each pandemic introduced a new subtype of influenza A virus into the human population. Because people had no immunity to the new subtypes, infection rates were very high, resulting in the spread of the viruses around the world within 1 year of detection. All three pandemics were traced to viruses that originated in birds and could be considered to be zoonotic diseases, that is, diseases that originate as an animal disease, but also are capable of causing disease in humans.

Avian Influenza

All known subtypes of influenza A viruses have been recovered from birds living in an aquatic environment, and these birds are considered to be the natural reservoir. Avian influenza (AI) viruses are carried asymptomatically by ducks, geese, and shorebirds; they typically do not exhibit any signs of disease. These bird species are the perfect disseminators of influenza A viruses worldwide because they migrate for long distances, spreading viruses through contaminated feces. 
Pathogenicity is a measure of the degree of illness that AI viruses cause in chickens. By the current definition from the Office International des Epizooties (OIE) in France, highly pathogenic avian influenza (HPAI) viruses cause death in at least six of eight experimentally infected chickens. In addition, if the genetic sequence of the AI virus in question is similar to that observed for other HPAI strains, then the virus must be
considered to be highly pathogenic, whether or not it causes overt disease. All other AI viruses are considered to be of low pathogenicity (LPAI) (Swayne and Halvorson 2003). This definition of the ability of these viruses to make chickens sick does not apply to humans or human infections with AI viruses. The HPAI viruses are considered to be foreign animal diseases (FADs) in the United States, meaning that they do not normally occur here and they are required to be reported to the state veterinarian’s office and to the U.S. Department of Agriculture–Animal and Plant Health Inspection Service (USDA–APHIS) immediately after detection. To date, all recorded HPAI viruses have been of the H5 or H7 subtypes. The LPAI viruses are endemic to the United States, exist in wild waterfowl and live-bird market reservoirs, and occasionally infect commercial poultry flocks. The LPAI viruses of the H5 and H7 subtypes also are reportable to state authorities because of their historical ability to mutate to the highly pathogenic form.
High pathogenic AI infections cause severe economic losses to affected poultry producers and are, therefore, considered an emergency disease requiring immediate eradication efforts. 
Surveillance systems currently are in place in the United States that focus on detecting AI viruses in poultry. Detection and rapid response are key elements of the U.S. AI control program. The National Poultry Improvement Plan (NPIP), a program of USDA–APHIS in cooperation with the poultry industry, monitors breeder birds (parents) of commercial egg-type chickens, meat-type chickens, and meat-type turkeys for the
presence of antibody to AI viruses. The NPIP currently is establishing a monitoring program for table egg chickens, meat-type chickens, and meat-type turkeys. The NPIP program tested 390,000 AI samples from commercial poultry in 2003 to assure the U.S. poultry industry and their trading partners that poultry products in the United States are free of AI. In addition, many state diagnostic laboratories routinely test backyard and commercial birds presented with respiratory disease signs for the presence of AI. For example, the state of North Carolina tested almost 200,000 birds in 2004 and Georgia tested 100,000 birds in 2003. The USDA–APHIS is developing an AI monitoring program for the live-bird market system in the northeastern United States. 
This early detection must be complemented with rapid and complete containment plans. Avian influenza outbreaks involving low pathogenic strains of the H5 and H7 subtype generally are handled at the state level. Plans to eradicate H5 and H7 strains in poultry flocks have been developed in most poultry-producing states. These plans are widely disseminated and are activated immediately upon detection of one of these strains. These procedures allow poultry producers to protect their investments by quickly eradicating an influenza virus before it becomes highly pathogenic.

Human Cases of Avian Influenza

In recent years, there were fewer than 100 reported human deaths worldwide associated with AI. Most of these deaths were attributed to the Asian HPAI (H5N1) virus that is circulating in parts of (Eurasian) Asia. Most human deaths attributed to Asian HPAI (H5N1) have occurred in Asian countries (Sims et al. 2005). It seems that the virus has spread beyond Asia as migratory waterfowl move to winter nesting grounds or through the movement of infected domestic fowl, but only a small number of human cases have been reported outside of Asia. The farming practices and culinary customs unique to Asia are believed to be associated with the transmission of AI viruses from birds to humans. In most of the human cases of Asian HPAI (H5N1), there was close contact with infected live or recently dead birds. There have been no human cases of Asian HPAI (H5N1) associated with eating properly cooked poultry meat or eggs. The Asian HPAI (H5N1) virus strain infecting humans can cause severe disease and death partly because humans have little to no immunity to the H5 subtype viruses. There have been fewer than 200 documented human cases of Asian HPAI (H5N1) resulting in fewer than 100 deaths during an 8-year period despite the probable exposure of millions of people in these countries, making the transmission of the virus from birds to humans rare. Human-to-human transmission of Asian HPAI (H5N1) has been limited and sustained human-to-human transmission has not been documented; however, each additional human case increases the chance that the virus eventually will improve its transmissibility in humans. The emergence of an Asian HPAI (H5N1) virus strain that is transmitted readily among humans could result in the start of a new pandemic.

Pandemic Risk Assessment

Asian HPAI (H5N1) remains primarily an animal disease. It is not easily transmitted from birds to humans and human-to-human transmission has not been shown to be sustained. The relatively few confirmed human deaths that have occurred worldwide reflect how rare this virus infection is in humans. During the 8-year period cited previously, approximately 288,000 Americans died from human influenza. Currently, the risk of humans contracting Asian HPAI (H5N1) is extremely low. The spread of Asian HPAI (H5N1) to poultry in additional countries is likely during waterfowl migration, through trade in the live-bird markets, and through the movement of infected domestic fowl, especially ducks. Heightened surveillance for waterfowl die-offs and outbreaks in poultry flocks is needed to quickly identify virus spread and to initiate response programs. Because the Asian HPAI (H5N1) virus is highly pathogenic in most poultry species and some wild birds, disease detection should not be difficult in most cases, provided adequate diagnostic capability is available. Domestic ducks, however, have been shown to be asymptomatic carriers of the virus and may serve as a silent reservoir for the disease. Heightened efforts to detect influenza viruses in asymptomatic birds are important to ensure early detection and eradication. Rapid depopulation and destruction of infected flocks followed by thorough cleaning and disinfection are essential in ensuring that Asian HPAI (H5N1) remains an animal disease and is eventually eradicated altogether. Intensified testing of flocks in close proximity to known positive flocks could prevent asymptomatic flocks from moving to processing or to other markets. Unfortunately, many at-risk countries in Eurasia, the Middle East, and Africa lack the necessary diagnostic and animal health infrastructure to adequately carry out surveillance for the presence of Asian HPAI (H5N1) and will require significant financial help from the more developed countries. 
Introduction of Asian HPAI (H5N1) to the United States could occur via infected birds or infected humans. Because the United States does not import live birds or poultry products from countries where the Asian HPAI (H5N1) has been reported, the most likely bird source for Asian HPAI (H5N1) would be migratory waterfowl or illegally smuggled birds. Birds migrating into and out of the Asian HPAI (H5N1) endemic areas are not likely to be an issue in the United States until spring migration and the return of birds to summer nesting grounds. The eastern-most flyways for migratory birds in Asia do include the Arctic and Alaska, although no positive birds have been detected there to date. Increased surveillance along these flyways could facilitate early detection if Asian HPAI (H5N1) were to be introduced. No major poultry-producing regions exist in the Arctic or in Alaska, but the west coast of Canada and of the United States (Washington, Oregon, and California) are potentially at risk. 
Heightened human surveillance for signs of severe respiratory disease should be implemented, especially for those people traveling to or from endemic areas or those living there. Reporting of human cases of respiratory diseases and more intensive testing for influenza A viruses could provide early detection in the unlikely event that human infections occur. 
Different farming systems are associated with the differing risks of both bird infection and human infection. Birds grown in modern enclosed housing are at a much lower risk of contracting AI from wild birds than are birds raised outside. Modern U.S. farm production practices provide for more control over the movement of poultry and allow for the implementation of strict biosecurity procedures designed to prevent the introduction of disease agents to domestic flocks. In addition, commercial poultry raised in integrated agricultural systems typically are grown on farms dedicated to a specific processing plant and are not sold or commingled in livestock markets. Effective surveillance systems and veterinary oversight help decrease the risk of spreading AI viruses in commercial poultry in this country. This modern type of poultry production is more protective of birds and their health than traditional agricultural systems in which birds are raised in small flocks outside, a system that is commonly found in countries in the developing world. The spread of Asian HPAI (H5N1) in Southeast Asia is mostly occurring in small villages where poultry, especially domestic ducks, are raised in open air fields with exposure to wild migratory birds and then sold live in village markets (Sims et al. 2005). This practice promotes the maintenance of the virus reservoir in domestic ducks and leads to recurring infections.


The Asian HPAI (H5N1) remains primarily an animal agriculture disease today. Eradication of this disease needs to occur at the farm level in the countries where it is currently circulating. Adequate federal funding of prevention, surveillance, and eradication efforts in Asia and in the at-risk countries outside of Asia not only will facilitate the eradication process if this virus is detected but also will prevent further spread and subsequent economic loss to the affected country and decrease the opportunity for the virus to adapt to humans. Every new poultry infection, and subsequent human exposure, gives this virus an opportunity to exchange genetic material with other influenza viruses, including human influenza subtypes, and increases the chances that Asian HPAI (H5N1) will become a significant human disease. Education of U.S. citizens about the relatively low risk of becoming infected with Asian HPAI (H5N1) virus is needed to calm the fears of a pandemic created by the almost constant media publicity on this issue. 


Antigenic. Having the properties of a substance that induces a specific immune response; usually resulting in the production of antibodies that prevent future disease from specific organisms.
Antigenic drift. Small, gradual changes in the genetic make-up of the virus resulting from errors in copying the genetic material.
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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.
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