Marek’s Disease by Dr. Darrell W. Trampel, D.V.M., PhD.

Marek’s Disease

 Darrell W. Trampel, D.V.M., PhD.
Iowa State University
January 27, 2014

Marek’s disease (MD) is a highly contagious disease of chickens characterized by a) varying degrees of paralysis of wings and legs and/or b) development of lymphoid tumors.  Marek’s disease is found in broiler chickens raised for meat and in laying hens maintained for egg production.  “Range paralysis” is an old, but very descriptive name for MD.  With this condition, chickens are unable to walk and tend to lie with one leg stretched forward and the other back.  Paralysis of one or both legs is caused by accumulation of neoplastic lymphocytes in nerves which causes structural damage and nerve enlargement.  Death often results from starvation and dehydration because paralyzed chickens are unable to reach food and water.  After 3 weeks of age, chickens may develop tumors (lymphomas) in almost any tissue or organ.  Chickens with lymphomas frequently become depressed, stop eating, often have pale shriveled combs, and become emaciated prior to death.  Marek’s disease tumors are gray-white in color and may appear as distinct nodules or as a diffuse infiltration that makes the affected organ look paler than normal.

Marek’s disease is a form of cancer caused by a herpesvirus (Gallid herpesvirus 2).  Marek’s disease viruses are placed into categories based upon their ability to produce disease.  These categories include mild, virulent, very virulent, and very virulent plus strains of Marek’s disease virus.  The virus initially infects and destroys B lymphocytes which causes a transient immunosuppression.  However, most neoplastic cells present in tumors consist of CD4+ helper T lymphocytes.  In addition to paralysis and tumors that are the most common manifestations of MD, several other syndromes occur.  Immunosuppression develops in the early stages of infection due to destruction of B lymphocytes that normally produce antibodies.   Skin leucosis results from accumulation of neoplastic lymphocytes around feather follicles.  “Gray eye” describes the appearance of chicken eyes after MD tumor cells have infiltrated the iris and cornea and results in blindness.   Atherosclerosis in chickens is caused by MD virus and closely resembles chronic human atherosclerosis.  Atherosclerosis is an accumulation of cholesterol‑filled plaques on the inner walls of blood vessels which reduces the diameter of the vessel lumen.  Transient paralysis is caused by MDV-induced damage to blood vessels in the brain with subsequent leakage of fluid into the surrounding brain tissue.  Temporary swelling of the brain causes chickens to develop nervous tics and twisted necks.

Marek’s disease virus in large numbers are shed in keratinized feather follicle epithelial cells (dander) that slough off the surface of the skin of infected chickens and are disseminated by air currents.  Shedding begins 2 to 4 weeks after infection, prior to the appearance of clinical disease, and can continue for the life of the chicken.  Dander protects the virus from physical degradation and contaminated poultry house dust remains infectious for at least 4‑6 months at room temperature.  Dander is a major component of poultry dust and inhalation of keratinized epithelium containing MD virus is the major route of infection.  Chickens may contact residual dust and dander in the growing house from a previous flock or dust from adjacent chicken houses.  Poultry dust can remain infectious for over a year.  Contaminated dander may be spread from one location to another on undisinfected eggs, contaminated clothing, shoes, equipment, and vehicles.  Feather tips contain MD virus and darkling beetles can carry the virus from one location to another.  Once introduced into a house, infection spreads quickly from bird to bird.  Transmission through the egg does not occur.

Prevention requires a combination of good hygiene and vaccination.  Chicks placed in a contaminated environment are likely to be infected within the first few days of life.  Delaying the time of exposure allows more time for development of the chick’s immune system and immunity following vaccination in the hatchery.  Up to 7 days is required for solid immunity following vaccination.  Failure to prevent early exposure is the most common cause of vaccine failure.  Exposure to MD virus can be delayed and the challenge dose diminished by careful cleaning followed by disinfection of the brooder house prior to chick placement.  Thorough cleaning is an essential first step because droppings, dust, and other organic matter remaining on surfaces will inactivate disinfectants.  Chicks should be housed in a building that do not contain older chickens.  Older chickens are likely to be shedding MD virus and represent a potential source of infection for baby chicks.

Marek’s disease vaccine was the first practical effective cancer vaccine in any species of animal and represented a major scientific advance in medical science.  The first commercial vaccine against MD was the herpesvirus of turkeys (HVT, serotype 3) introduced in 1971 and still widely used today.  HVT can still be obtained as a cell-free lyophilized vaccine that does not need to remain frozen to maintain potency.  HVT became less effective as MDV in the field became more virulent.  In the early 1980’s, bivalent vaccines containing HVT and naturally non-oncogenic serotype 2 MDV became available.  Serotype 2 vaccine viruses include strains SB-1 and 301B/1.  Serotype 3 vaccine (HVT) and a serotype 2 vaccine (SB-1 or 301B/1) have synergistic activity when combined and administered together.  During the 1990s, field strains of MDV became even more virulent and a serotype 1 vaccine was employed to generate higher levels of immunity.  This vaccine (Rispins, CVI988) was developed at the Central Veterinary Institute in the Netherlands and is now widely used in the United States and around the world.   Serotype 1 and 2 vaccines are cell-associated vaccines and consist of frozen, viable MDV-infected cells that require storage and transport in liquid nitrogen.  MD vaccines can be administered subcutaneously on the back of the neck at 1 day of age or in fertile eggs (in ovo) at 18 days of incubation.  More broilers in the United States are vaccinated by the in ovo method.

Vaccination of chicks to prevent Marek’s disease is strongly recommended.  Marek’s disease vaccines are not perfect, but they are very effective.  In most hatcheries, the cost of Mark’s disease vaccination is 19-20 cents per chick –  money well spent to prevent a widespread disease of chickens.

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4 Time Olympic Triathlete teams up with Murray McMurray Hatchery

Four Time Olympic Triathlete and Seven Time U.S. Elite National Champion, Hunter Kemper, has joined with Murray McMurray Hatchery to promote backyard chickens and fresh, backyard eggs.

Hunter and his family recently received newly hatched chicks from Murray McMurray Hatchery in Webster City, Iowa.  The Kemper family will start enjoying fresh eggs from their own chickens within approximately 16 weeks.  As Hunter continues to train and monitor his nutrition, the value of a nutritious fresh egg will fit well into his diet.  “The egg is the standard when it comes to a natural form of protein,” says Hunter.  “By having our own chickens, I know what they are being fed, how they are being treated, and I love the idea of eating fresh eggs right from my backyard.  My family and I are looking forward to getting our first egg.”

Murray McMurray Hatchery will be showcasing Hunter’s adventure with his new chicks throughout the year at  .  The Kemper family will be posting pictures, videos and blogs about their experiences as they learn how to care for the chicks.  Fans of Hunter Kemper and chicken lovers alike will be able to ask questions of Hunter and offer him advice on caring for the chickens.

“When Chris (Chris Huseman, Director of Marketing for Murray McMurray Hatchery) and I first started talking, I didn’t realize how popular raising your own chickens is,” explains Hunter.  “I love the idea that my family now can help play an integral part in my nutrition as we all share in the fun of raising our own chickens.  My boys absolutely loved getting the chicks – they have not stopped smiling about them.”

With his five new breeds of chickens, Hunter Kemper will be aiming for his record breaking fifth U.S. Olympic team at the 2016 RIO Olympic Games.

Murray McMurray Hatchery has been providing family memories with newly hatched chickens, turkeys, geese, ducks and other fowl since 1917.  The company offers more than 100 breeds of chickens and other fowl and serves customers throughout the entire United States.  More information about Murray McMurray Hatchery can be found at

Hunter Kemper is a Four Time Olympic Triathlete and Seven Time U.S. Elite National Champion.     Hunter and his wife, Val, live in Colorado Springs, CO with their three boys and baby girl.   More information on Hunter can be found at   You can follow Hunter on Twitter at @hunterkemper.

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The Arrival by Hunter Kemper

Chris called us last week to let us know that our chicks would be arriving – this is great as our kids would all be home for their delivery.  The anticipation was great as the boys, especially our oldest son Davis (7 years old), could not wait to meet our new baby chicks.

Saturday morning came, and they were determined to meet the mail lady at the front door.  It was a very warm January day, so the kids waited outside on the front stoop.  They waited and waited.  The mail lady actually came to deliver our mail, but no chicks.  I thought they might arrive on a separate truck perhaps.  So they waited some more.  Finally, around 2:00pm, I called our local post office looking for our chicks.  They had not seen them.  They figured their transit was probably slowed by the weather in Iowa.  The kids were bummed.  We were a little worried that the chicks would suffer if they didn’t arrive until Monday.  However, we talked to the people at Murray McMurray and they assured us that the chicks would be fine.  Apparently it is very common for it to take a few days for the chicks to arrive.  We felt reassured that the chicks would be ok.

The next morning, we were all ready to go to church when there was a knock on the door.  It was the mail man and he had our chicks!  I had no idea U.S. Postal Service delivered on Sunday.  Apparently they make some exceptions, and this was one of them!  What an exciting surprise to start off our Sunday morning.

Watch this movie trailer which features our new adventure raising our chicks:

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Preparing a Home by Hunter Kemper

Our brooder set-up!

Our brooder set-up!

Murray McMurray Hatchery has helped make the preparation for our chickens very easy.  Their
book: “Chickens in Five Minutes a Day” is awesome!  It’s an easy read and tells you everything you need to know about raising chickens.  We also got one of their starter kits.  This kit included a roll of cardboard to create the brooder guard, 2 containers for the water, 2 feeders, an infrared bulb to heat the brooder, and a thermometer to help keep the correct temperature.  We got the brooder set up in the storage room in our basement, laid some soft pine bedding down, and prepared a home for our baby chicks.  We have started learning about the different breeds we were going to be getting.  We are prepared, and getting really excited for the day our chicks arrive.  Our kids (we have a 2 month old girl and 3 boys – ages 7, 3 1/2, and 2) are especially excited and counting down the days until the baby chicks arrive in the mail.

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Backyard Chicken Farmer – by Hunter Kemper

Backyard Chicken Farmer?

If you told me a few months ago that I’d be raising chickens in my backyard, I wouldn’t have believed you.  In my backyard?  Chickens?   It all sounded a little crazy to me until I spoke with Chris Huseman, Director of Marketing from Murray McMurray Hatchery in Webster City, Iowa.  First of all, I didn’t realize how popular backyard chicken farming was.  I thought you had to live on a farm to raise chickens.  I soon learned that this was not the case at all.  Many people actually raise their own chickens in cities and neighborhoods all across the U.S.  I started talking to my friends about it and learned that many of them had a true desire to raise their own chickens.  After talking to even more people, I’ve realized that I know a handful of people that are already raising their own chickens.  This was all new news to me.  The more I learned, the more interested I became.

After talking to Chris, and reading some books, I learned how easy it really was to raise chicks.  They need food, water, and a safe clean shelter.  I thought, I can do that.  I also liked the idea that raising these chickens would help teach my boys some daily responsibility as they help care for the chicks.   Finally, as a professional triathlete, I eat a lot of protein to help my body recover in between workouts.  Eggs are one of my favorite sources of protein.  So the thought of having my own fresh, organic, eggs daily sounded great!  People have told me that once you begin to eat fresh eggs straight from the hen, you will never go back to store bought eggs.  I can’t wait to try them!

So we made the decision, my family was going to become Backyard Chicken Farmers!

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Laryngotracheitis by Darrell W. Trampel, D.V.M., PhD.


 Darrell W. Trampel, D.V.M., PhD.
Iowa State University
January 6, 2014

         Each year, chicken owners contact me to discuss a serious disease in their chickens characterized by difficult breathing, loud wheezing, and gurgling.  Affected chickens often stand with heads and necks extended as they attempt to inhale.  Many owners report that their sick chickens are “gaping” with beaks wide open as they attempt to breathe.  When owners of backyard flocks are asked if new birds were added to their flocks during the weeks preceding onset of illness, they usually answer “yes.”  Owners of exhibition chickens frequently confirm that their birds have been to a fair, show, or swap meet in the recent past.  Almost always, new chickens added to the flock and other chickens displayed by other owners at exhibitions and sales were clinically normal and showed no signs of disease.  The flock history described above is typical for chickens experiencing infectious laryngotracheitis (ILT).


ILT is caused by a herpesvirus.  The time between exposure and onset of disease (incubation period) ranges from 6 to 14 days.  Disease within a flock may last for 2 or more weeks.  Nearly 100%  of chickens in a susceptible flock may become ill and mortality may reach 70% or more.  In addition to the symptoms described above, chickens with the severe form of the disease may violently shake their head and expectorate blood‑tinged mucus on walls.  The inner surface of the eyelids may be infected (conjuncitivits) and yellow exudates may accumulate beneath the eye lids.  Chickens may die suddenly with few previous signs of disease and egg production may decline by 10‑20%.   The trachea may contain blood, or if the chicken survives longer, a yellow mat of fibrin closely adhered to the inner surface of the trachea.  In many cases, the yellow exudate dislodges from the tracheal wall and causes a plug which obstructs the opening to the trachea (glottis) and the bird dies of asphyxiation.


Sources of infection include direct or indirect exposure to acutely affected birds and recently recovered carriers.  ILT virus replicates in the trachea for the first 7 days of an infection and virus shed in respiratory secretions from infected chickens heavily contaminate the environment.  Movement of contaminated litter, crates and coops, trucks, egg flats, and equipment can spread this virus from pen to pen, house to house, and farm to farm.  People can carry ILT virus on their hands, clothing and shoes, and are major contributors to transferring this disease from one location to another.  Wild free-flying birds, rodents, and insects are not infected themselves, but can act as mechanical carriers in dissemination of this virus.  Up to 50% of chickens that recover from this disease may be carriers because of the establishment of a latent infection and can shed ILT virus for up to 16 months.  Latent virus is found in the trigeminal ganglia where the ILT genome is integrated into the host DNA which allows the ILTV to evade the immune system.  Reactivation of latent virus and subsequent re-excretion occurs following stress associated with rehousing, mixing with unfamiliar birds, onset of egg production, and molting.  Egg transmission does not occur.


Prevention is of paramount importance because there is no specific treatment.  Antibiotics are sometimes used to prevent secondary bacterial infections, such as E. coli, but have no effect on viruses.  Backyard flocks kept for meat or egg production should be kept isolated.  Common mistakes, such as introducing recently vaccinated birds or adding birds obtained from a friend or auction should be avoided.  These chickens may appear normal but are potential ILT carriers.  Owners should never visit neighboring poultry flocks, especially those suspected of having a contagious disease.  Avoid borrowing equipment from other flock owners.  All used equipment brought onto a premises should be cleaned and disinfected prior to use.  Chickens should be transported in plastic crates or carriers which can be cleaned and disinfected.  ILT virus is readily killed by common disinfectants containing glutaraldehyde or quaternary ammonium.  However, ILT virus is resistant to disinfectants in the presence of organic matter, so thorough cleaning prior to disinfection is essential.


Vaccination early in an outbreak is feasible because of the long incubation period and relatively slow spread through a flock.  Two types of attenuated live vaccines are available, chicken embryo-origin (CEO) or tissue culture-origin (TCO) vaccines.  Immunity may develop by 3-4 days and persists for 15 – 20 weeks.  Vaccination by eyedrop provides more uniform flock protection than water or spray administration.  CEO and TCO vaccines may regain virulence as a result of passages in poorly vaccinated flocks or after reactivation from latency.   Outbreaks of ILT associated with prior use of tissue culture origin TCO vaccine are infrequent, but have been associated with CEO vaccines on multiple occasions.  CEO and TCO vaccines can be transmitted from vaccinated to unvaccinated chickens and may establish latency in apparently healthy chickens.  Consequently, vaccination is recommended only where the disease is endemic.  CEO and TCO vaccines transmitted to unvaccinated chickens do not protect contact-infected chickens.  In recent years, recombinant vaccines have become commercially available that are produced with a herpesvirus of turkeys (HVT) or fowl pox vector.  Recombinant vaccines do not replicate in the trachea and do not completely prevent replication of field strains in the trachea, so vaccinated chickens can shed field strains of ILTV.  Vaccination of backyard flocks is necessary only in areas where ILT is common.  In such flocks, all birds must be vaccinated.  Vaccination of exhibition fowl is strongly recommended when ILT is prevalent in an area.

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A Coccidiosis Primer

A Coccidiosis Primer

Darrell W. Trampel, D.V.M., PhD.
Iowa State University
December 26, 2013

Coccidiosis is found wherever chickens are raised.  Coccidiosis is an intestinal disease caused by protozoan parasites which belong to the genus Eimeria.  Disease occurs primarily in chicks that are 3 to 6 weeks of age and immunity develops in birds that survive.  By sexual maturity, most chickens have been infected and have developed immunity.  Coccidiosis is found in flocks ranging in size from a few chickens in a backyard environment to large commercial flocks containing thousands of broiler or egg-type chickens.  Chickens raised in cages, on floors, and on range are all susceptible to Eimeria coccidia.  Seven species of Eimeria cause coccidiosis in chickens, with E. acervulina, E. maxima, and E. tenella being the most common.  Coccidia have several stages in their life cycle, but the stage most important for transmission is the oocyst.  Oocysts are shed in droppings of infected birds and have a thick wall that enables them to survive in the environment for 18 months or longer.  Oocysts are not immediately infective after being shed, but must undergo a process called sporulation before they can cause disease.  Under favorable conditions, oocysts are capable of maturing within 48 hours and infecting other birds. The severity of coccidosis is proportional to the number of oocysts ingested.  Because of their thick wall, oocysts are resistant to disinfectants but are eventually killed by the action of ammonia, bacteria, and molds in litter.  Heat generated by litter composting (131 F), freezing, and drying will also kill oocysts.


Transmission.  Fecal-oral transmission takes place when oocysts shed in feces are consumed by a susceptible chicken.  Oocysts from infected chickens are shed in droppings and contaminate litter, feed, and water.  Susceptible chickens ingest Eimeria oocysts when they peck at litter, eat contaminated feed, or consume contaminated water.  Numbers of oocysts in litter usually peak when chicks are 4 – 5 weeks of age and then decline due to development of immunity in the chickens and toxic effects of the litter.  Oocysts can be mechanically carried from farm to farm, house to house, and pen to pen by externally contaminated people, equipment, insects, wild birds, and rodents.  Airborne fecal dust can transfer viable oocysts from one location to another.


Clinical and Subclinical Disease.  Coccidiosis may cause clinical or subclinical disease.  Chickens with clinical coccidiosis have severe diarrhea and are obviously sick.  Mild diarrhea causes fecal pasting around the vent and loose droppings can be seen on the surface of litter.  Severe, watery diarrhea may soak into litter and be difficult to see.  Diarrhea causes loss of water through the droppings and chickens rapidly become dehydrated.  Death losses in affected flocks typically peak  around 5 to 7 days after onset of diarrhea. Subclinical coccidiosis is not severe enough to cause overt illness but may markedly reduce the rate of growth and impair digestion and absorption of nutrients from feed.   Coccidiosis damages cells lining the inner surface of the intestinal tract and makes chickens susceptible to secondary diseases.  Proliferation of Clostridium perfringens bacteria in the intestinal tract is often associated with coccidiosis and causes a disease called necrotic enteritis.


Coccidia are host-specific.  Eimeria species typically infect only one avian species.  Chicken coccidia infect only chickens and will not infect other birds, such as turkeys, quail, or house hold pet birds.  And the opposite is true as well.  Coccidia that infect turkeys, quail, or wild birds will not infect chickens.  Because of host specificity, chicken coccidia do not pose a threat to the health of children, dogs, cats, other avian species, or livestock.


Chicken coccidian are site-specific.         Each Eimeria species infects a specific segment of the avian intestinal tract.  Location of coccidia lesions in the intestinal tract is somewhat helpful in identifying the species of Eimeria responsible for an infection.  For example, E. acervulina infects the upper intestinal tract (duodenum), E. maxima infects the mid-gut, and E. tenella infects the ceca.  Unfortunately, oocyst morphology and the location of different Eimeria species in the intestinal tract may overlap.  In addition, chickens may be infected by more than one Eimeria species at the same time.  Consequently, other tests, such as polymerase chain reaction (PCR), are needed to confirm the identity of specific Eimeria infections.  Affected segments of the intestinal wall are ballooned and may have a red and white speckled appearance.  In severe cases, intestinal contents may be watery or bloody and the inner surface of the intestine may be covered by a yellow-brown membrane.


Immunity against coccidiosis is species-specific.  Infection by one Eimeria species induces immunity only against that particular species, not against other Eimeria strains.  Because immunity is species-specific, it is possible for the same flock to experience several outbreaks of coccidiosis, each outbreak caused by a different Eimeria species.  Cell-mediated immunity mediated by T lymphocytes is the major mechanism for conferring resistance to cocccidiosis, not antibodies.


Chickens suffering from coccidiosis may or may not have blood in their droppings.    The presence or absence of blood in droppings depends primarily upon the species of Eimeria causing the infection and the number of oocysts ingested.    Eimeria acervulina, E. maxima, E. mitis, and E. praecox infect surface epithelial cells and cause malabsorption but do not cause bloody droppings.  In contrast, E. tenella, E. necatrix,  and E. brunetti  penetrate deep into the intestinal wall and damage blood-filled capillaries which causes hemorrhage in the intestinal wall and bloody droppings.


Treatment.  Coccidiosis in chickens can be treated with amprolium or sulfonamides.


Preventive Management.  Good management is important to limit oocyst sporulation in the litter and recycling through chickens.  Oocysts survive longer in high moisture environments which allow higher numbers of coccidia to survive in the litter.  Temperature and ventilation in chicken houses should be used to keep litter dry (30 – 40% moisture).   Water spillage from drinkers should be minimized and wet litter (cake) should be removed from around feeders and waterers to avoid a build-up of high concentrations of sporulated oocysts.  Waterers should be cleaned at least once per day and overcrowding of birds should be avoided.  If coccidiosis has been a problem, thoroughly remove used litter between flocks and start new flocks on clean litter to minimize the number of oocysts encountered by baby chicks.


Preventive Medication and Vaccination.  Coccidiosis can be controlled by using preventive drugs (coccidiostats) or by vaccination.  Two broad groups of anticoccidial feed additives are available, ionophorus antibiotics or synthetic chemicals.  Ionophorous antibiotics are incorporated into the Eimeria cell membrane and facilitate transfer of cations across the membrane and into the cytoplasm of coccidia.  Coccidia parasites must use energy to remove cations and excess water.  When stored energy reserves are depleted, the coccidia cell swells with water and dies.  Feeding medicated chicken feed containing amprolium is the easiest method available to prevent coccidiosis in small flocks.


         Vaccines have had success comparable to medication, but vaccine application must be carefully controlled and careful, continuous management of litter is critical.  Vaccinated chicks are exposed to a small controlled dose of virulent live oocysts that initiate infection and induce an immune response.  Vaccine sporulated oocysts with a colored dye are given to day old chicks in the hatchery using a specially designed spray cabinet.  The dye allows hatchery workers to monitor vaccine coverage and encourages preening and ingestion of live oocysts.  A different vaccine delivers sporulated oocysts to chicks in an edible gel puck that can be placed in chick boxes at the hatchery or on feed trays in the poultry house.  Delivering too high a dose to chicks may cause disease and providing too few oocysts results in lack of immunity.  Approximately 6 – 9 days after vaccination, fresh oocysts are excreted into the litter.  Birds must ingest sporulated oocysts from litter to stimumulate further immunity, so litter conditions must permit the proper amount of sporulation.  If litter is too dry, sporulation and recycling may be insufficient to provide continued stimulation of the immune system.  If litter is too wet, sporulation may be excessive and clinical disease may occur.  Food and water provided before vaccination and for at least 21 days after vaccination must not contain anticoccidial drugs.

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Pullorum Disease, Poultry, and the NPIP by Dr. Darrell W. Trampel, D.V.M., PhD.

 Pullorum Disease, Poultry, and the NPIP
Darrell W. Trampel, D.V.M., PhD.
Iowa State University
December 2, 2013

          Development of purebred chickens can be traced back to 1875 when the American Poultry Association (APA) published a book entitled “Standards of Perfection” which promoted purebred breeds of chickens.  Unlike randomly mated chickens, purebred chickens produced offspring that closely resembled the parent birds and had predictable physical appearance and egg production.  This predictability made purebred flocks more profitable than outbred flocks.  However, in 1916, the International Baby Chick Association (IBCA) was formed as a trade association of hatchery operators following a philosophical disagreement with the APA.   APA members wanted to breed chickens for their form and color and selected breeding birds based upon judging at shows.  Hatchery operators wanted to breed chickens to produce more eggs and selected breeders on the basis of performance testing.  The IBCA sponsored egg-laying contests.

The poultry industry began to grow in the early 20th century, but a disease known as Bacillary White Diarrhea limited the early expansion of the industry.  This disease, later called Pullorum Disease (PD), was rampant in poultry and could cause upwards of 80% mortality in recently hatched chicks.  Some chicks died before hatching and others died a week or two after hatching with white urates on top of watery droppings.    Poultry producers were unable to cope with this disease until the cause was identified and methods of detection and prevention were developed.  In 1899, the bacteria that caused bacillary white diarrhea, now called Salmonella Pullorum, was discovered.  Ten years later, it was learned that this bacteria could be transmitted from one generation of chickens to the next through contaminated eggs – a novel concept at the time.  By 1913, a blood test was developed that made it possible to test breeder flocks and eliminate reactors so pullorum disease could eventually be eradicated from a flock.  When testing began in 1914, 9.8% of chickens tested were reactors and investigators learned that more than a single test of a flock was necessary to detect and remove all infected individuals.


The potential for rapid, nationwide spread of PD increased dramatically with the emergence of mail-order hatcheries and large, forced-air incubators.  In 1918, the U.S. Postal Service first accepted baby chicks to be shipped by parcel post.  Poultry breeders who developed chickens with superior production capabilities were besieged with orders for baby poultry from all over the country.  The first large electric incubator was developed by Petersime in 1923.  Large incubators provided air movement and uniform temperatures and facilitated expansion of the poultry industry.  These large incubators frequently contained hatching eggs from multiple breeder flocks at the same time.  S. Pullorum from contaminated eggs produced by positive breeder hens was found to be transmitted during the hatching process to clean chicks sharing the same hatching tray.  PD disease was probably introduced into commercial turkey flocks by co-mingling chicken eggs and turkey eggs in forced-draft incubators.  This finding stimulated research to improve hatchery sanitation.


Ensuring that chicken breeding stocks were free of PD was a major motivation for development of the National Poultry Improvement Plan (NPIP).  Groundwork for development of the NPIP was laid at the 1933 IBCA Convention in Grand Rapids, Michigan.  Members agreed upon standard terminology for the breeding and hatching industries to describe different degrees of freedom from PD.  They also adopted a Code of Fair Trade Practices and, because of unethical practices by some members, asked the federal government for help in regulating their industry.  On July 1, 1935, the NPIP became operational after being established by an act of Congress.  Provisions were based upon recommendations from the IBCA.  The NPIP immediately began inspecting hatcheries for S. Pullorum and contaminated hatcheries were shut down.  In addition, the NPIP operated the U. S. Record of Performance program which publically listed how different breeds performed in egg-laying contests.  Use of the stained-antigen, rapid, whole-blood test to detect and eliminate breeders infected with Salmonella Pullorum probably did more than anything else to improve the quality of chicks.


Today, the NPIP is a voluntary Poultry Industry-State-Federal program for prevention and control of egg-transmitted, hatchery-disseminated poultry diseases, such as PD.  Participation in all NPIP programs is voluntary, but all flocks, hatcheries and dealers must qualify as “U.S. Pullorum-Typhoid Clean” before participating in other NPIP programs.  Participating flocks are listed in the official NPIP Directory of Participants which identifies states, flocks, hatcheries, and dealers that meet disease control standards specified in the Plan’s programs.  As a result, customers can buy poultry that has tested clean of certain diseases or that have been produced under disease-prevention conditions.  In addition, participating flocks have an approval number which can be used on shipping labels, certificates, invoices, and other documents.  Provisions for hobbyist and exhibition waterfowl, exhibition poultry, and gamebird breeding flocks are found in Subpart E of the NPIP.


Pullorum Disease is still common in Mexico, Central and South America, Africa, and parts of Asia.  S. Pullorum has adapted to chickens and typically produces acute systemic disease characterized by sudden death and high mortality only in very young chicks.  Infection of baby chicks frequently results in a persistent carrier state in clinically normal surviving chickens.  S. Pullorum persists and survives within the spleen and liver.   At the onset of egg production, physiological changes and a surge in sex hormones causes transient immunosuppression and allows a resurgence of infection.  During this period, numbers of S. Pullorum  bacteria increase in the liver and spleen of carrier hens and spread to the ovary and oviduct.  Infected hens have reduced egg production and eggs have reduced fertility and hatchability.  Reproductive tract infection of hens leads to shedding of S. Pullorum in up to one third of eggs laid and transmission to chicks that hatch from contaminated eggs.  Infected chicks shed S. Pullorum in their feces which contaminate feed, water, and litter.  Transmission to pen-mates occurs rapidly due to ingestion of contaminated feed, water, and litter.   S. Pullorum may survive for years in a favorable environment and may be carried by rodents.


Thanks to efforts by the NPIP, Pullorum Disease is now rare in the United States.  Even though chickens are the natural host, turkeys may be infected as well and infections are usually lifelong.  Occasionally, S. Pullorum is isolated from unusual hosts, such as ducks, guinea fowl, pheasants, quail, sparrows, canaries, bullfinches, parrots, and peafowl.  Even wild turkeys have yielded positive tests in a few instances.  No drug or combination of drugs will eliminate infection from a flock, so it is important to prevent vertical transmission from hens to chicks via contaminated eggs.  This goal is accomplished by identifying clinically normal carrier breeding chickens by testing with the stained-antigen whole blood test.  This test detects antibodies in the bloodstream which are directed against S. Pullorum.   To ensure adequate time for antibodies to develop in infected poultry, minimum ages at testing have been established.  Chickens should be more than 4 months of age when tested, turkeys more than 12 weeks of age, and upland gamebirds more than 4 months of age or after attaining sexual maturity, whichever comes first.   Minimum number of poultry to be tested is 30 birds per house, with at least 1 bird taken from each pen and unit in the house.  In houses containing fewer than 30 birds, all birds in the house must be tested.  The ratio of male and female birds tested must be the same as the ratio of male to female birds in the flock.  Positive tests must be reported to the State Animal Health Official (usually the State Veterinarian) and to the Official State Agency (NPIP office) in your state.


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2013 Fall Photo Contest Winners

Congratulations to our winners of the 2013 Fall Photo Contest!

1st Place Winner

1st Place Winner

2nd Place Winner

2nd Place Winner

3rd Place Winner

3rd Place Winner

4th Place Winner

4th Place Winner

5th Place Winner

5th Place Winner

6th Place Winner

6th Place Winner

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Poultry: The Gateway Farming Enterprise by Joel Salatin

Note:  In his recent book, FIELDS OF FARMERS:  INTERNING, MENTORING, PARTNERING, GERMINATING, Joel Salatin describes multi-generational, symbiotic farming opportunities.

With the average American farmer nearing 60 years old and half of all farmland slated to change hands within the next 15 years, we have both an unprecedented problem and an unprecedented opportunity.  The problem, of course, is inter-generational succession:  who will farm this land?

The opportunity is that half of all U.S. agriculture assets are owned by people 60 years old and up, which means that multi-generational partnerships are ripe for development.  It means that land, buildings, and machinery are not being utilized as much as they could be.

When we look at economic sectors, if young people can’t get in, then old people can’t get out.  That’s exactly what we have in today’s farming conundrum.  Many farmers are nearing their exit, but too few are coming on behind them to fill those vacancies.  We desperately need incoming opportunities, or what I call gateway enterprises, that
are easy for young farmers to enter.  Healthy economic sectors need fluidity between the generations to create ultimate sustainability.

As I see it, direct marketed pastured poultry is one such gateway.  The reason is that Americans are eating chicken:  it’s an everyman, everyday food, not some exotic once-in-awhile food tasting experiment.  The bigger the buying pool, the more marketable the product.

Second, poultry is a low capital enterprise.  You don’t need much acreage, much infrastructure, or much equipment.  With portable shelters and lightweight electric netting or feed trailers, you can get in with minimal investment.

Third, poultry enjoys a quick cash turnaround.  Goodness, an eight week broiler start to finish is about as fast as a radish.  That means a well-run enterprise can cash-flow expansion and the payback on initial investment is quick.  Compare that to even a whole-season grain crop or something long like cattle.

Fourth, poultry is family friendly.  You don’t have to worry about a wayward bull running over a child.  Even if a chicken pecks your finger, it may hurt, but it won’t break skin or send you to the emergency room.  Even a child is bigger than a chicken.

Fifth, the inputs for poultry are easy to find.  With many good hatcheries to choose from and plenty of cottage-scale processing equipment now available, entering the business is easy and not daunting.

As a complementary business to an existing farm operation, perhaps nothing is more versatile than pastured poultry.  Whether a farm is orcharding, cropping, or livestocking, pastured poultry enterprises fit symbiotically into the landscape without competing with the mother business.  That means that literally all the production currently
concentrated in poultry factories could be divested throughout America’s farmland on decentralized entrepreneurial operations operated by a new generation of self-starting farmers who don’t have high capitalization costs.

In such a scenario, older farmers who desperately need young blood would enjoy the enthusiasm, ideas, and energy of these partnering farmers.  Both generations benefit and the whole society enjoys soil building, landscape healing pastured poultry.  How many young people–and some not so young–sit at their Dilbert cubicles every day
dreaming about a full-time farming enterprise?  It’s doable.  The time is now.  Never has the opportunity beckoned as temptingly.  It’s time to answer the call and do it.  Now is the time to build these successional, sustainable, multi-generational partnerships.

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