1. Lymphoid leukosis
Dr. Chi-Young Wang

2. It is called big liver because the liver is usually enlarged with nodular tumor.
Species: Chickens and exotic birds.
Action: Chronic, it takes weeks for disease to occur.
Age of bird-It occurs usually in 16-week-old birds or older except for osteopetrosis. Osteoperosis occurs in broiler-age birds.

3. Etiology
RNA virus in the family of retrovirus. Five viral subgroups (A-E) are known.
ALV was inoculated into day-old chicks and obtained a tumor response in 200–270 days. In these transmission experiments, all sources of virus that cause LL also caused erythroblastosis. Osteopetrosis, hemangiomas, and fibrosarcomas were also observed in chickens of certain strains and passages.

4. Model of transmission
It spreads through the eggs (transovarian). It is a ubiquitous organism in commercial poultry flocks.
Shedding of ALV into egg albumen and transmission to the embryo is a consequence of virus production by albumen secreting glands of the oviduct. The congenitally transmitting ALV, the highest titers of virus were found in the ampulla of the oviducts.

5. Model of transmission

6. Model of transmission
Exogenous ALVs are transmitted in 2 ways: vertically from hen to progeny through the egg and horizontally from bird to bird by direct or indirect contact. Only a small percentage of chicks are infected vertically, this route of transmission is important.

7. Model of transmission
Although vertical transmission is important in the maintenance of the infection, horizontal infection may also be necessary to maintain a rate of vertical transmission sufficient to prevent the infection from dying out.

8. Model of transmission
Four classes of ALV 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-.

9. Model of transmission
The susceptible birds in an infected flock fall into one of the other three categories. Most are V-A+, and a minority, usually less than 10%, are V+A-. Most V+A- hens transmit ALV to a varying but relatively high proportion of their progeny. A small proportion of V+A+hens transmit the virus congenitally and do so more intermittently.

10. Model of transmission
Congenitally infected embryos develop immunologic tolerance to the virus and after hatching make up the V+A- class, with high levels of virus in the blood and tissues and an absence of antibodies. The susceptible birds in an infected flock fall into one of the other three categories.

11. Clinical Signs
Signs include paleness, emaciation, weakness, and inappetence.
Tumors are internal. The abdomen is enlarged and feather are sometimes spotted with urates and bile.
The feed/gain ratio is decreased,
Increased culls and decreased egg production occurs.

12. Postmortem lesions Peripheral nerves are never involved.
Bursa are always enlarged and may contain nodular tumor.
The infection persists longer in bursal lymphocytes than in other hematopoietic tissues and cells of the bursa of Fabricius are the target cells that neoplastically transform.

13. Postmortem lesions
Visceral tumors are soft, smooth, and glistening. Tumors may be nodular, miliary, or diffuse. Tumors are common in gonads, lungs, liver, spleen, heart, kidney, mesentery, and bone marrow.
A proliferation of lymphoblasts occurs in lymphoid follicles in the bursa. These altered bursal follicles are termed transformed follicles and is regarded as a focal preneoplastic hyperplasia.

14. Postmortem lesions

15. Postmortem lesions
The miliary form, which is most obvious in the liver, consists of numerous small nodules less than 2 mm in diameter uniformly distributed throughout the parenchyma.
Nodules in the liver are surrounded by a band of fibroblast-like cells that have been remnants of sinusoidal endothelial cells. In the bursa, a follicular pattern of tumor growth usually can be seen.

16. Postmortem lesions

17. Postmortem lesions Tumors consist of aggregates
of large lymphoid cells
(lymphoblasts) that are all
at the same early
developmental stage.
They have a poorly defined
cytoplasmic membrane,
much basophilic cytoplasm,
and a vesicular nucleus.

18. Postmortem lesions
The skin is never affected and skeletal muscles often contain tumors.
Eyes are never affected.
Bone sometimes contains tumors.
The blood often contains tumors.
Fat tumors are common (Liposarcoma).

19. Postmortem lesions
Erythroid leukosis occurs in birds around 3 months. The liver, kidney, and spleen are enlarged. The enlarged organs are usually cherry red, soft, and friable. The marrow is hyperplastic and red in color.
With severe anemia, atrophy is seen in visceral and lymphoid organs like spleen. The blood is watery and light red and clots slowly.

20. Postmortem lesions
The marrow in early cases reveals blood sinusoids filled with rapidly proliferating erythroblasts that fail to mature. Varying degrees of anemia may occur. Extramedullary erythropoiesis is common.

21. Postmortem lesions
For myeloblastosis, the liver is enlarged and firm with diffuse grayish tumor infiltrates. The spleen and kidneys are infiltrated and enlarged. The bone marrow is replaced by a solid, yellowish-gray tumor cell. A severe leukemia exists, with myeloblasts comprising up to 75% of peripheral blood cells and forming a thick buffy coat.

22. Postmortem lesions The liver shows a massive
intravascular and extravascular accumulation of myeloblasts.
In the spleen, these tumor cells
accumulate in the red pulp and
the bone marrow, myeloblastic
activity is confined to
extrasinusoidal areas.

23. Diagnosis Tumors in adult birds are characteristic for this disease.
Liposarcoma are also characteristic.
The complement fixation for avian leukosis virus or ELISA tests are conformatory. Histopathology reveals large lymphoblasts in tumors. Lymphoblasts have a ovoid nucleus and a finer, more delicate chromatin network.

24. Diagnosis
The complement fixation and ELISA tests use specific serum to determine the presence of the organism in blood, tissue, serum, vaginal swab or egg albumin.
It stimulates E. coli, aspergillosis, MD, tuberculosis, erythroblastosis, and myeloblastosis.

25. Diagnosis
Most leukosis viruses replicate in fibroblast cultures without producing any obvious cytopathic effect. Their presence can be detected by a variety of tests. ALVs of subgroups B and D may induce cytopathic plaques that may be used for virus assay.

26. Diagnosis
Application of eradication programs of ALV to commercial flocks has depended on associations between virus infections in hens, eggs, embryos, and chicks:
(1) Egg albumen may contain exogenous ALV and gs antigen, and both are usually present together.
(2) A strong association exists between ALV or gs antigen in egg albumen and ALV in vaginal swabs.

27. Diagnosis
(3) An association exists between ALV in vaginal swabs or egg albumen and ALV in chicken embryos and newly hatched chicks.
The ELISA test (p27 antigen) to albumen or swabs is the need to differentiate positive reactions due to the presence of gs antigen derived from endogenous or exogenous ALV infection. Reactions due to the latter are usually markedly higher.

28. Diagnosis A procedure for eradication of ALV involves:
(1) selection of fertile eggs from hens negative in the egg albumen or vaginal swab test
(2) hatching of chicks in isolation in small groups in wire-floored cages, avoidance of manual vent sexing, and of vaccination with a common needle to prevent mechanical spread of any residual infection

29. Diagnosis
(3) testing of chicks for ALV by a biologic assay or PCR on blood, discarding reactors and contact chicks
(4) rearing ALV-free groups in isolation
Some commercial breeder organizations are concentrating only on reduction of infection rate by hen testing.

30. Prevention and Treatment
Select birds that are leukosis virus negative using serologic methods to prevent spread of the disease.
None treatment.

31. Special Note
It is immunosuppressive and a major cause of condemnation in adult broiler breeders and layers.