It's another beautiful day on the farm, and having fed and watered the horses, cows, sheep, and other assorted barnyard animals, you decide to drive on over to take care of the real moneymaker, your chicken houses. Breathing in the heavy perfume of poultry, you open the door to your house... only to find that mortality has been steadily increasing, your birds are looking rather bumpy, and everyone's looking a little worse for the wear. What's going on here? You can shake your Magic 8 ball, or you can keep reading- it looks like you're going to need to know everything you can about Avian Leukosis.

Same shtick, different virus

Avian Leukosis is a neoplastic disease caused by the (aptly named) Avian Leukosis virus (ALV). This is a retrovirus of the genus Alpharetrovirus. It features multiple subgroups labeled by different letters. Of medical importance to the poultry industry are A, B, C, D, E, and J. These different serotypes can manifest in different diseases, in different birds, with different results. The virus replicates within the host cell after shedding its envelope, utilizing reverse transcriptase to change its RNA information into usable DNA. In the case of ALV-E, this DNA inserts into the genome of the host cells and remains there for the remainder of the bird's less than comfortable life. It's said to be 'endogenous'. This is of particular concern when discussing vaccines derived from chick embryos, such as the human vaccine for measles and mumps. The CDC recently had indications that ALV-E might be included in vaccines produced in eggs- this was discounted by a battery of molecular tests. I haven't read anything stating that any of these diseases are zoonotic, but you never want to pop a new RNA virus into anyone, just in case. At any rate, all other forms of the disease are exogenous- they just infect the bird without getting inside it's cellular head. The virus itself is pluripotential- this means that it can produce completely different types of tumors determined by the dose, type, age of bird, and various other factors.

The two important subcategories we need to focus on are ALV-A/B, and ALV-J. These little buddies are in the same family, but cause variable diseases in different types of birds. Most birds have some resistance to subtypes A and B, but ALV-J is a newly emerging threat, meaning most birds are susceptible. Disease associated with ALV-A/B takes about 16 weeks to incubate. ALV-J may heat up in a range from 3-17 weeks.

Well where did this come from?

Unlike Marek's disease, vertical transmission is the biggest player in moving this virus into the population at large. When a hen becomes infected with the virus, either during or previous to the onset of lay, she includes virus, through transovarian transmission, in the eggs she is laying. As the virus develops along with the cells of the embryo, chickens hatching from these eggs will not be able to differentiate the virus from their own cells. They become shedders for life. These birds will shed virus in their feces, which can infect other birds laterally through the fecal-oral route. This is especially important during young life, right after hatch. Another important vertical transmission method is seen more commonly with ALV-J. In this case, the transmission is not through transovarian infection, but rather contamination of the egg shell by the infected mother. Upon hatch, chicks are exposed to the virus and become infected. Birds can become infected from other birds throughout their life, resulting in differing levels of infection and transmission status. This is especially true of ALV-J, which appears to have an advanced knack for spreading between birds. Those birds lucky enough to be infected later in life usually become, at worst, intermittent shedders, and at best, shed virus for a short period of time before mounting an effective immune response. Vertical transmission paints a very poor picture for the parents infected with the virus, but we'll get to that a bit later on.

How have I offended the Poultry Powers-that-be? Why my birds?

This is a good time to start differentiating between the diseases caused by ALV-A/B and ALV-J.

Lymphoid Leukosis:

  • This manifestation of the disease occurs when the bird is infected with ALV-A or B subtypes of the virus. This is a disease that affects commercial layers and meat producing chickens.
  • This is the form of the disease that has a general incubation period of about 16 weeks, which means that it is a disease of older birds.
  • This is not a disease of broilers (the progeny of broiler-breeders), who only live to an age of about 4-6 weeks. The “meat producing” birds are therefore not the ones whom the meat is being taken from, but rather, the birds making the birds who'll be slaughtered. This includes many genetic generations of birds, due to the intensive nature of poultry breeding programs.
  • We're talking about chickens, here. Turkeys aren't really at risk.

Myeloid Leukosis:

  • This manifestation of the disease occurs with the ALV-J subgroup. This is a disease of meat chickens, not layers.
  • Because it has an incubation of 3-17 weeks, it can be seen to possibly affect broilers. However, it is more likely that it affects the parent flocks of those broilers, due to the length of incubation.
  • Again, we're not talking turkeys. Turkeys will get theirs later.

Well how do I know if it's a leukosis at all? What should I be looking for?

The two types of leukosis will present different symptoms, because they're just complicated that way. In general, you can expect your birds to be:

  • Depressed
  • Emaciated
  • Dying at a low, chronic level-- There is no huge peak in mortality to signify disease. There is just a long-term chiseling away of your live bird population that exceeds normal mortality rates.

Each disease is found with its own characteristic lesions. Here's a few to pick over:

  • Lymphoid Leukosis-
    • B cell lymphoma-- tumors in/on the Bursa of Fabricius may be seen, indicating B lymphocyte involvement by the virus. This can have profound effects for young birds, as the bursa is an immune organ. If it, or the B cells it produces, are destroyed by virus, the bird will show immunosuppression throughout life.
    • Visceral tumor-- tumors may appear on the liver or other abdominal viscera, such as the heart and ovaries.
    • Grossly enlarged liver (hepatomegaly)-- the liver may grow large enough to fill the entire abdominal cavity. This is often referred to as “big liver” disease in the hens it infects.
  • Myeloid Leukosis-
    • Myelocytoma-- Basically, a collection of immature leukocytes that has gotten together to form a little tumor/growth. It is essentially a little leukemia, which is never good. Diagnostic myelocytomas will form on the larynx of the bird, and will be visible when opening the beak.
    • Osteomyelitis-- an infection/tumor of the bones. These will form in the bones of the skull, which will appear early in the infection as bumps on the head. These form quickly and are easy to see because the bones of the cranium are so thin.
    • Characteristic Tumors-- Tumors also occur on the trachea and on the underside of the sternum. These are VERY characteristic lesions.
    • Decreased egg production
    • Decreased growth rate/uniformity-- because some birds may be affected at different rates or may not be infected, or have variable lesions, feed conversion goes out the door and some birds may be runted, stunted, and otherwise unwanted in the production system.

All right, you've got me. But what if you're wrong?

Differential diagnoses are, as always, horribly important. Let's take a look at a few of the most pressing.

If the bursa has not regressed, we know it can be any of the differentials above. However, if the bursa features tumors rather than just being present, we can assume that the disease is not IBD. We know that this disease presents tumors, but does not have any nerve or other neurological involvement, meaning it's probably not Marek's or REV. Death is slow, not acute, creating another downvote for REV. Fowl Pox would probably be accompanied by dry lesions as well as wet lesions, so if it's not there, it's not there. And the bumps of Fowl Cholera and Colibaccilosis are bone infections, not tumors. A bacterial swab and culture should reveal the culprit.

So if we are looking at chronic mortality and tumors and a huge liver and decreased productivity, it's safe to say we're looking at an Avian Leukosis. Further differentiation can be based on the specific symptoms noted above. There are laboratory tests that can be done and even personal testing kits available from IDEXX and other manufacturers that can be used to verify the presence of the virus. Lab work can even tell you what serotype it is, just to make sure. Take a look at the first source below for some interesting work being done in Australia.

Okay. So. I hate to admit it, but you're probably right. What's going to happen?

Myeloid leukosis can have a big impact on the economic value of your flock. Birds are going to die, which obviously costs money. Production value is lost because infected broilers are unable to process and convert feed at the rate of their uninfected brethren, resulting in poor uniformity, higher cull rates, and low investment/return ratios for growers, who are trying to save money at every turn. Production is also lost in the form of eggs. Older birds can't be sold after they exit production because they'll be riddled with tumors. Layers and broiler-breeders with Lymphoid leukosis will also have a very low resale rate. All in all, things are looking down. Plus, we've got to talk about the costs of trying to control this thing.

Oh hell. What do we do to control it?

Unfortunately, there's no such thing as “treatment” for this disease. What is done instead is to attempt to eradicate the disease from the population. This generally involves virus testing in parent, grandparent, and great-grandparent flocks. If the disease is located at any level within this system, it's most likely that the tier above it is infected. This means that to eradicate vertical transmission, that flock must be destroyed. This process has been used to great effect in the eradication of other prevalent vertically transmitted diseases, such as the mycoplasmas. This is extremely costly as it is essentially destroying entire genetic lines of birds- if the most meatiest, laid-back birds are the ones infected with this virus, they've still got to go, and it's back to the genetic drawing board all over again. Unfortunate, but necessary. Currently, uninfected flocks are being sought to attempt to look at the possibility of a vaccine.

In general, testing and surveillance is the preferred method of prevention. If your birds don't have the disease, then they haven't got the disease, and that's good news. If they get it, you can quickly spot it and weed it out before it propagates. Good hygiene practices are also important, including biosecurity between flocks and houses and sanitization of the facilities between cycles. As always, it's a poor idea to keep different age birds in the same house. This is one of the confounding factors for Lymphoid leukosis affecting layers, who are often reared in multi-age facilities. All in, all out, people! Save yourself the heartache!

So that's what I've got.

Join us again soon for the continuing saga of debilitating, horrendous immunological challenges facing today's modern chicken on the go.

Sources:
  • http://www.rirdc.gov.au/reports/CME/04-116.pdf http://www.cdc.gov/ncidod/eid/vol7no1/hussain.htm
  • http://www.thepoultrysite.com/diseaseinfo/11/avian-leukosis-lymphoid-leukosis-leukosis-sarkoma-group
  • Mad props for the WebCT notes provided by my dear Dr. Stephen Collett and the ever-impressive stand-in presentation and handouts given by Dr. Guillermo Zavala, who's studies are quoted in the first link up there. Continuity! w00t!

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