89. Avian leucosis and reticuloendotheliosis.

Question 1

Avian Leukosis Occurrence?

Answer 1

Avian leukosis Suscetible:

• Chicken (mainly), hen, turkey, pheasant
• Retroviridae, Orthoretrovirinae, Alpharetrovirus, Avian leukosis virus
• Leukosis sarcomatosis virus complex ʹ high variability
• Forms:
• Lymphoid leukosis = most frequent
• Erthroblastosis
• Myeloblastosis
• Fibrosarcoma, hemangioma, nephroblastoma, osteopetrosis

Occurrence:

• worldwide,
• clinical forms less frequent,
• in large-scale farms more frequent,
• eradication

Question 2

Ethiology of Avian Leukosis?

Answer 2

Etiology:

• Alpharetrovirus genus
• Avian leukosis viruses:
• Subgroups (envelope):10 subgroups A-J (chicken mainly = A, B, C, D, E,J) J is pathogenic!
• Based on envelope proteins
• Viruses originating from avian leukosis virus: deletion, recombination Æ avian sarcomatosis,
• myeloblastosis virus, erythroblastosis virus
• Rous-sarcoma virus: has onc-gene, rapid oncogenesis (can become defect and lose own oncogene)
• Antigen:
• p27 (core, group specific ʹ used in diagnostics)
• p85 (surface protein, binding) ʹ very variable ʹ cannot have vaccine to cover all strains
• All oncogenic: malignant transformation of host cells
• some have their own onc gene: FAST
• some only activate the onc gene of the host cells: SLOWER oncogenesis
• Can be cultured (embryonated egg, tissue culture)
• Low resistant: enveloped
• Different type of tumors can be caused by the same virus

Question 3

Epidemiology of avian leukosis?

Answer 3

Epidemiology

• Widespread, shedding with feces and saliva, persistantly infected birds maintain and shed, slow spread
• (need close contact)
• Infection:
• Vertical: germinative/vertical infection (immune tolerance, persistent infection) ʹ infected
• day old chick hatch
• Horizontal: day-old chicken, 1st week, shed will decrease then stop, if yolk immunity good
• will shed less
• Appearance of tumor is influenced by:
• origin of virus, amount of virus, way of infection, age, gender, immune state, resistance
• against tumor - certain species (animal with clinical tumor is low <4%)

Question 4

Pathogenesis of avian Leukosis?

Answer 4

Pathogenesis:

• infection (germinative or MM) > viremia > replication in organs > tumors (if hatched with infection,
• immunotolerant, day-old infection, inhibited by antibodies, different tumor types)
• Resistance: cellular resistance to infection (resistant to second infection)
• Immune response: cytoT lymphocytes, the later the infection = the better the immune response
• Lymphoid leukosis:
• Bursa Fabricii > B lymphocytes (<2 months: more severe)
• Development of tumor after 2-4 months (slow)
• Metastases (in sexually matured animal): liver, spleen, kidney
• Lesions in animals > 4-5 months old (long incubation period)
• Erythroblastosis: virus replicate in erythroid cells of bone marrow, producing immature RBC, anemia
• Myeloblastosis: myeloblast cells transformed
• J-subtype: higher diversity, higher virulence
• Meat-type poultry
• Replication in myelocytes in bone marrow: myeloblastoma, hemangioma
• Other diseases: fibrosarcoma, nephroblastoma, osteopetrosis
• Rous-sarcoma: own onc-gene, malignant transformation in CT around body (fast tumorformation)
• Osteopetrosis: thickening of long bone

Question 5

Pathology of Avian Leukosis?

Answer 5

Pathology:

• Lymphoid leukosis: enlarged liver and spleen, greyish-white uniform tissue of liver, spleen (mottled), kidney,
• bone marrow, bursa fabricii, fiber of CT (strong tissue), diffuse or focal lesions
• Erythrosis: liver, spleen, bone marrow - cherry red
• Myeloid leukosis: greenish-grey tumor tissue
• J-type: tumor in parenchymal organs, tumors in bones and cartilage
• Histology: identify cell type

Question 6

Diagnosis and differentiation?

Answer 6

Diagnosis:

• clinical signs, PM lesions, histology
• Detection of virus: PCR
• Detection of group-specific antigen (p27) = ELISA, COFAL (complement fixation for avian
• leukosis)
• Virus isolation: tissue culture, egg
• Detection of the antibodies ilf ( Can’t confirm the diagnosis)

Differentiation:

• Marek disease (age, proportion of T and B lymphocytes - marek is mostly T lymphocytes
• and leukosis is mainly B lymphocytes, MATSA)
• Reticuloendotheliosis (lab examinations)
• J-subgroup virus (tumor in bone and cartilage)

Question 7

Prevention/Control of avian Leukosis?

Answer 7

Prevention, control:

• To reach disease-free stock
• Older hens: infected eggs are less frequent
• Resistance selection
• Eradication: selection for genetic resistance, with selection (test and slaughter)
• Selection of virus shedders (detection of virus or antibodies)
• Isolation of negative chicken
• Examination of shedding the virus
• Prevention of re-infection
• No vaccines

Question 8

Reticuloendotheliosis Occurence and susceptible species?

Answer 8

Reticuloendotheliosis

• Retroviridae, Orthoretrovirinae, Gammaretrovirus, Reticuloendotheliosis virus A,T

Occurrence:

• widespread,
• present in Hungary,
• not as frequent as avian leukosis
• *Susceptible**:
• turkey (main), chicken, geese, ducks

Question 9

Ethiology of reticuloendotheliosis?

Answer 9

Etiology:

• Gammaretrovirus genus: related retroviruses
• Reticuloendotheliosis virus REV type A and T
• Chicken syncytial virus
• Duck spleen necrosis virus
• Host: turkey (mainly), chicken, geese, ducks
• REV virulence variants:
• REV-T: oncogen (defected virus - incomplete virus) - own onc-gene, fast developing tumor
• REV-A: helper (not defected virus - complete virus) - immunosuppression, growth retardation don’t
• have its own onc-gene, slow developing tumor
• 1 serotype - 3 subtypes

Question 10

Pathogenesis of reticuloendotheliosis?

Answer 10

Pathogenesis:

• infection: germinative, PO, aerogenic,viremia
• Highly oncogenic: RES, tumor transformation of lymphoid cells, tumor in different organs
• Less oncogenic: immune suppression, prolonged course ʹ slower
• Immune response: viremia, shedding can be limited

Question 11

Clinical signs of reticuloendotheliosis?

Answer 11

Clinical signs:

• incubation time 3 days - 3 months (depending on virulence: REV-T shorter, REV-Alonger)
• General signs: depression, anorexia, diarrhea, anemia
• Retardation: abnormal feathering, decreased weight gain
• CNS signs: locomotion precipitation
• Skin, MM precipitation, immune suppression

Question 12

Pathology of reticuloendotheliosis?

Answer 12

Pathology:

• Tumors: diffuse or solitary, liver, spleen, heart, kidney, ovarium
• Stomach: ulceration, hemorrhages
• Thymus, bursa atrophy
• Thickened peripherial nerves (edematous)

Question 13

Diagnosis and prevention of reticuloendotheliosis?

Answer 13

Diagnosis:

• epi, clinical signs, PM lesions
• Detection of virus: IF, ELISA, PCR, virus isolation
• Detection of antibodies: iIF, ELISA
• Differentiation: lymphoid leukosis, marek disease
• Prevention:
• Introduce only disease-free animals
• difficult to eradicate (selection of shedding parents, eliminate seropositive day-old chicken)
• no vaccines