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Lymphoid Leukosis in Poultry

(Avian leukosis)

By John Dunn, , USDA-ARS

Under natural conditions, lymphoid leukosis has been the most common form of the leukosis/sarcoma group of diseases seen in chicken flocks, although in the 1990s myeloid leukosis become prevalent in meat-type chickens. The International Committee on Taxonomy of Viruses placed viruses of the avian leukosis/sarcoma group in the Alpharetrovirus genus of the family Retroviridae.

Members of this RNA group of viruses have similar physical and molecular characteristics and share a common group-specific antigen. Detection of the major antigen (p27) present in the core of leukosis/sarcoma viruses forms the basis of several diagnostic tests. Lymphoid leukosis occurs naturally only in chickens. Experimentally, some of the viruses of the leukosis/sarcoma group can infect and produce tumors in other species of birds or even mammals. The infection is known to exist in virtually all chicken flocks except for some SPF flocks from which it has been eradicated. Tumor mortality commonly accounts for ~1%–2% of birds, with occasional losses of ≥20%. Subclinical infection, to which most flocks are subject, decreases several important performance traits, including egg production and quality. The frequency of infection has been reduced substantially in the primary breeding stocks of several commercial poultry breeding companies, particularly egg-type breeders. In recent years this control program has expanded, and infection has become infrequent or absent in certain commercial flocks. The frequency of lymphoid leukosis tumors even in heavily infected flocks is typically low (<4%), and disease is often inapparent. As much as 1.5% excess mortality per wk has been reported in commercial broiler-breeder flocks naturally infected with subgroup J avian leukosis virus.


Lymphoid leukosis is caused by certain members of the leukosis/sarcoma group of avian retroviruses. Isolates that can induce lymphoid leukosis in chickens are commonly called avian leukosis viruses and are divided into subgroups A, B, C, D, and J, on the basis of differences in their viral envelope glycoproteins, which determine antigenicity, viral interference patterns with members of the same and different subgroups, and host range. Subgroups A and B are most prevalent in western countries. Since the initial isolation of subgroup J avian leukosis virus in England, the virus has been isolated from broiler-breeder stocks that experience myeloid neoplasms (myelocytoma) in many other countries. A sixth subgroup (E) designates nononcogenic endogenous viruses produced by viral genes integrated into the host cell DNA. All field strains of avian leukosis virus are oncogenic, although some differences in oncogenicity and replicative ability have been recognized. Recently, recombinant avian leukosis viruses with the envelope of subgroup B and long terminal repeat of subgroup J have been isolated from field cases of myeloid leukosis in commercial layers. Another recombinant avian leukosis virus with the envelope of subgroup A and long terminal repeat of subgroup E was shown to be a contaminant in commercial Marek’s disease vaccines. Thus, recombination between two different subgroups of avian leukosis virus can occur in field conditions and cause economic losses.

Transmission and Epidemiology:

Chickens are the natural hosts for all viruses of the leukosis/sarcoma group; these viruses have not been isolated from other avian species except pheasants, partridges, and quail. Avian leukosis virus is shed by the hen into the albumen or yolk, or both; infection probably occurs after the onset of incubation. Congenitally infected chickens fail to produce neutralizing antibodies and usually remain viremic for life. Horizontal infection after hatching is also important, especially when chicks are exposed immediately after hatching to high doses of virus, eg, in feces of congenitally infected chicks or in contaminated vaccines. Horizontally infected chickens have a transient viremia followed by antibody production. The earlier the infection, the more likely it is to lead to tolerance, persistent viremia, and tumors. Other factors known to increase the susceptibility of chickens to horizontal infection include the absence of maternal antibodies and the presence of endogenous retroviruses, especially those associated with the late feathering (K) gene. Tumors are more frequent in congenital than in horizontal infections, but many more chickens are exposed horizontally than congenitally. Rates of embryo transmission typically are 1%–10%; virtually all chicks in an infected flock are exposed by contact. Congenital and, in some cases, early horizontal infection can induce permanent carrier states characterized by shedding of virus or antigen into the environment and into eggs. Late infection (ie, inoculation at 12–20 wk of age) is unlikely to lead to viral shedding.

Four classes of avian leukosis virus infection are recognized in mature chickens: (1) no viremia, no antibody (V-A-); (2) no viremia, with antibody (V-A+); (3) with viremia, with antibody (V+A+); and (4) with viremia, no antibody (V+A-). Birds in an infection-free flock and genetically resistant birds in a susceptible flock fall into the category V-A-. Genetically susceptible birds in an infected flock fall into one of the other three categories. Most are V-A+, and a minority, usually <10%, are V+A-. Most V+A- hens transmit the virus to a varying but relatively high proportion of their progeny.

The virus is not highly contagious compared with other viral agents and is readily inactivated by disinfectants. Transmission can be reduced or eliminated by strict sanitation. After the infection is eradicated, standard disease control and sanitation practices can keep chicken flocks free of the disease. The role of males in transmission of avian leukosis virus is uncertain. Infected cocks apparently do not influence the rate of congenital infection of progeny but act only as virus carriers and sources of contact or venereal infection to other birds.


Lymphoid leukosis is a clonal malignancy of the bursal-dependent lymphoid system. Transformation invariably occurs in the intact bursa, often as early as 4–8 wk after infection. Tumors are often not detectable until ~14 wk of age. Death rarely occurs before 14 wk of age and is more frequent around the time of sexual maturity. The disease can be prevented, even up to 5 mo of age, by treatments that destroy the bursa. The tumors are composed almost entirely of B lymphocytes that, in many instances, have IgM on their surfaces. No antitumor immune response has been recognized. Antibodies are readily induced after infection, except when tolerance occurs.

The induction of lymphoid leukosis tumors can be enhanced in chickens coinfected with serotype 2 Marek’s disease virus, a common vaccine virus. This enhancement requires a genetically susceptible chicken and early infection with lymphoid leukosis virus in addition to serotype 2 Marek’s disease vaccination. Because most commercial chicken strains are resistant, and lymphoid leukosis virus infection has been largely eradicated from susceptible stocks, enhancement is not currently recognized as a field problem.

A subclinical disease syndrome characterized by depressed egg production in the absence of tumor formation is more important economically than are deaths from lymphoid leukosis. Chickens with subclinical disease usually shed virus or viral antigen into the albumen of eggs. The pathogenic mechanisms are poorly understood.

Clinical Findings and Lesions:

Chickens with lymphoid leukosis have few typical clinical signs. These may include inappetence, weakness, diarrhea, dehydration, and emaciation. Infected chickens become depressed before death. Palpation often reveals an enlarged bursa and sometimes an enlarged liver. Infected birds may not necessarily develop tumors, but they may lay fewer eggs.

Diffuse or nodular lymphoid tumors are common in the liver, spleen, and bursa and are found occasionally in the kidneys, gonads, and mesentery. Involvement of the bursa has been considered virtually pathognomonic, although bursal lymphomas are also known to be induced by reticuloendotheliosis virus. Sometimes the bursal tumors are small and seen only after careful examination of the mucosal surface of the organ. Usually, no enlargement of peripheral nerves is apparent, although such lesions have been noted after experimental inoculation of subgroup J virus. Microscopically, the tumor cells are uniform, large lymphoblasts. Mitotic figures are frequent.

Outbreaks of neoplasms other than lymphoid leukosis such as myelocytomas, hemangiomas, and renal tumors have also been noted in meat-type chickens infected with subgroup J avian leukosis virus. Myelocytomatosis and skeletal myelocytomas may cause protuberances on the head, thorax, and shanks. Myelocytomas may occur in the orbit of the eye, causing hemorrhage and blindness. Hemangiomas may occur in the skin, appearing as “blood blisters,” which may rupture and bleed. Renal tumors may cause paralysis due to pressure on the sciatic nerve. Microscopically, in cases of myelocytomas induced by subgroup J avian leukosis virus, the liver shows a massive intravascular and extravascular accumulation of myeloblasts characterized by the presence of cytoplasmic eosinophilic granules.

Most strains of leukosis/sarcoma viruses also induce nonlymphoid tumors (including sarcomas), erythroblastosis, myeloblastosis, myelocytomas, hemangiomas, nephroblastomas, osteopetrosis, and related neoplasms. The nature of the tumors and their frequency depend on virus strain, chicken strain, age, dose, and route of infection. Occasional outbreaks of predominantly one type of tumor are seen in the field. The Rous sarcoma virus, a member of this group, has been widely studied in the laboratory. Each strain usually causes a predominantly neoplastic disease and can be distinguished on the basis of pathogenicity. Some viruses (eg, Rous sarcoma and erythroblastosis viruses) contain a viral oncogene that enables the virus to induce neoplasms within a short incubation period, but such viruses are rare in the field. Others cannot replicate on their own and require a nondefective helper virus. In recent years, avian leukosis virus infection has been shown to be associated with the so-called “fowl glioma,” characterized by cerebellar hypoplasia and myocarditis.


Because avian leukosis virus is widespread among chickens, virus detection tests, including virus isolation and PCR and the demonstration of antigen or antibody, have limited or no value in diagnosing field cases of lymphomas. Gross characteristics of diagnostic significance include the tumorous involvement of the liver, spleen, or bursa in the absence of peripheral nerve lesions. The tumors are found in birds >14 wk old. Histologically, the lymphoid cells are uniform in character, large, and contain IgM and B-cell markers on their surface. Tumors can be differentiated from those of Marek’s disease by gross and microscopic pathology and by molecular techniques that demonstrate the characteristic clonal integration of proviral DNA into the tumor cell genome with the associated disruption of the c-myc oncogene. Lymphoid leukosis cannot easily be differentiated from B-cell lymphomas caused by reticuloendotheliosis virus except by virologic assays; however, such tumors probably are extremely rare. Several PCR primers specific for detection of the most commonly isolated avian leukosis viruses, particularly subgroups A and J, have been developed. Other primers specific for endogenous, subgroup E avian leukosis virus have also been used. PCR has been used to detect and characterize avian leukosis virus strains contaminating commercial live virus vaccines of poultry. ELISA kits for detection of antibodies to avian leukosis virus subgroups A, B, and J are available commercially.


Eradication of avian leukosis virus from primary breeding stocks is the most effective means to control avian leukosis virus infection and lymphoid leukosis in chickens. Breeder flocks are evaluated for viral shedding by testing for viral antigens in the albumen of eggs with enzyme immunoassays or by biologic assays for infectious virus. Eggs from shedder hens are discarded, so that progeny flocks typically have reduced levels of infection. If raised in small groups, infection-free flocks can be derived with relative ease. These control measures are applied only to primary breeder flocks. Voluntary programs to reduce viral infection have already reduced mortality from lymphoid leukosis and improved egg production in most layer strains; similar programs were equally successful in certain meat strains. Some breeders favor, and have virtually achieved, total eradication, while others favor a reduced level of viral infection. Some chickens have specific genetic resistance to infection with certain subgroups of virus. Although genetic cellular resistance is unlikely to replace the need for reduction or eradication of the virus, the cellular receptor gene has recently been cloned, and quick molecular assays for viral susceptibility could be developed. Thus far, vaccination for tumor prevention has not been promising.

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