AVIAN LEUKOSIS / SARCOMA VIRUS GROUP (ALSV)

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AVIAN LEUKOSIS / SARCOMA VIRUS GROUP (ALSV)

• It comprises a variety of transmissible benign
  and malignant neoplasms of chickens and caused by
  members of genus of avian retroviruses belonging
  to the family Retroviridae.
• Under natural conditions the most common form of
  neoplasms is the lymphoid leukosis (LL).
• Economic losses from ALS group of diseases come
  from two sources
• First mortality ranged from 1 to 2 and may
  reach to 20 or more.
• Second, subclinical infection by ALSV produces a
  depressive effect on performance especially egg
  production and quality.
• In addition, their suppressive effect on the
  immune response leading to increase the
  susceptibility to many diseases and vaccination
  failure.

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Etiology

• Avian leukosis viruses are members of the
  leukosis / Sarcoma (L/S) group of avian
  retroviruses.
• Based on properties for viral envelope
  glycoproteins, members of the L/S group including
  ALVs from chickens are classified into six sub
  groups A, B, C, D, E and J.
• No cross neutralization between different
  subgroups.

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Etiology

• Strain classification
• A B are the most common subtypes exogenous in
  the field.
• C D are the less common
  .
• E is the endogenous subtype of ALV.
• J is the exogenous subtype that infect broiler
  meat type chickens.

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Etiology

• Exogenous viruses ALVs transmitted as infectious
  virus particles.
• Endogenous viruses The almost normal chicken
  genome also contains several classes or families
  of avian retrovirus-like elements that are
  transmitted genetically. (Genetic transmission)

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Etiology

• Thermal Inactivation
• The half-life of various ALVs at 37oc for 260
  min. (4.3 hr.)
• The half-life of various ALVs at 50oc for 8.5min.
• The half-life of various ALVs at 60oc for 0.7min.
• PH ranged from 5 to 9.

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Transmission

• Chickens are the natural host. Rous sarcoma
  virus has the widest host range.  
• A-  Transmission of exogenous virus
• It occurs in two ways
• ?Vertically. Four serologic classes occur in
  mature chickens in relation to ALV infection
• 1- No viremia, no antibody (V-A-)
• 2- No viremia, with antibody (V-A)
• 3- With viremia, with antibody, (VA)
• 4- With viremia, no antibody (VA-).
• - 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
  absence of antibodies.

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Transmission

• Horizontal infection
• Shedding of virus from saliva, feces and semen of
  cock, to other birds.
• Blood sucking insects as the chicken red mite,
  the fowl tick, and mosquitoes.
• Live virus vaccine prepared from so-called
  normal embryos are potential source of spread
  of infection.

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Transmission

• Horizontal Transmission
• The cock acts only as a virus carrier and source
  of contact of venereal infection to other birds.
• 1/2- 1/8 embryos were infected from eggs with
  virus in the albumen.
• Virus particles are shed in droppings of newly
  hatched chicks.

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ALSVTransmission

• B-  Transmission of endogenous ALV
• Endogenous ALVs are usually transmitted
  genetically in germ cells of both sexes (vertical
  transmission). Endogenous viruses have little or
  no oncogenicity but may influence response of the
  bird to infection by exogenous ALV. 

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pathogenicity

• It differ according to
• Origin of virus
• Virus subgroup
• Virus dose
• Route of infection
• Age of host
• Genotype (genetic constitution) and sex of the
  host

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Clinical signs

• Non-specific
• According to the organs affected and the form of
  the disease
• Lymphoid leukosis
• Erythroblastosis
• Myeloblastosis
• Myelocytomatosis.
• Oesteopetrosis.
• One or more specific neoplasms induced by ALVs
  may occur in a given flock of chickens and more
  than one type of neoplasm may occur in an
  individual birds.

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Lymphoid leukosis (LL)

• It is the most common ALSV in birds. In field
  outbreaks, LL cases can occur any time after 14
  wk of age however, incidence is usually highest
  at about sexual maturity.
• Sings of LL are not specific, depression,
  inappetence, decrease in the production.
• Gross lesions of LL
• Tumors involve liver, bursa of Fabricius, spleen,
  kidneys, lungs, gonads, heart, bone marrow and
  mesentery.
• Tumors are soft, smooth and glistening.
• A cut surface appears grayish to creamy white and
  seldom has areas of necrosis.
• Nodular tumor, Miliry, diffuse or combination of
  these forms.
• Occasionally, the liver is firm, fibrous and
  almost gritty.
• Hematology
• Blood films reveal the presence of immature
  lymphoblasts and budded or pseudopoded
  lymphocytes in large amounts.

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criteria Lymphoid Leukosis (LL) Mareks Disease (MD)
Age It does not occur before 14 wk of age. Mortality occurs between 24 and 40 wk of age. It may occur as early as 4 wk of age. And increase condemnation rates. -Mortality peak varies from 10 20 wk of age.
Bursal lesion Nodular tumors of bursa. Intrafollicular tumors consisting of uniform large lymphocytes. In some birds, it induces a premature atrophy of bursa. In others, the bursa may be tumorous, in which case the wall may be thickened from interfollicular infiltration with pleomorphic lymphocytes.
Nerve lesion - Paralysis with gross lesions of peripheral nerves. Lymphoid infiltration in nerves.
Eye lesion - Gross lesions of iris (gray eye) with lymphoid infiltration.
Skin lesion - Tumors in skin and/or muscles. Feathers follicular pattern of lymphoid cell infiltration in skin.
Infiltrating cells Homogeneous population of lymphoblasts. Immature lymphoblasts are highly pyroninophilic. LL tumors are composed of B cells and have surface IgM markers. Tumors usually contain lymphoid cells varying in size with maturity from lymphoblasts to small lymphocytes) and plasma cells. These medium and small lymphocytes do not stain with pyronin. 60-90 of tumor cells are T cells that lack IgM markers and only about 3-25 are B cells.
Tumor-associated cell surface antigen (MATSA) Absent in tumor cells. From 0.5-35 of tumor cells have MATSA.
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2. Erythroblastosis (Eb)

• It is usually seen in growing birds (over 3
  months of age) 3-6 months of age.
• It occurs in two forms
• Acute the blood is dark red with smoky overcast.
• Subacute the blood is watery, light red and
  clots slowly.
• Signs of Eb
• General weakness, emaciation, diarrhea and
  paleness due to sever anemia.
• Gross lesions of Eb
• There is usually a general anemia.
• Diffuse enlargement of liver, kidney and spleen.
  These organs are usually cherry red to dark
  mahogany and are soft and variable. While, marrow
  is hyperplastic, semi-liquid, cherry red and has
  hemorrhages.
• Petcheial hemorrhage on muscles, subcutis and
  viscera.
• Thrombosis infarction lead to rupture of liver
  or spleen
• Edema in lungs, heart (hydro-pericardium) and
  abdomen (Ascitis).
• Finally, atrophy of spleen and lymphoid organs.
  
• Hematology of Eb
• Stained blood smears reveal a variable number of
  erythroblasts, and immature cells of the
  myelocytic series. Hemoglobin content is reduce,
  plasma ratio is increased with sever low
  erythrocytes count.

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3- Myeloblastosis (Mb)

• It affects also growing birds.
• Signs are similar to erythroblastosis, but it
  have long coarse.
• The parenchymatous organs are enlarged and
  friable.
• in chronic cases the liver may be firm, nodular
  or diffuse tumor.
• Bone marrow is reddish gray to gray solid.
• In advanced cases, these organs appear mottled
  (morocco leather) or even granular.
• Hematology of Mb It is characterized by a
  spectacular leukemia. In the peripheral blood,
  myeloblasts may be found in a large number, may
  compose 75 of all blood cells.
• The disease may result in a secondary anemia, in
  which sever decrease of erythrocytes and plasma
  ratio with highly increase of leukocytes ratio
  (thick buffy coat).

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Myelocytomatosis

• It has a longer incubation period than Eb and Mb,
  but shorter than LL.
• General signs are similar to those of Mb and Eb.
  In addition, skeletal growth of myelocytes may
  result in abnormal protuberances of the head,
  thorax, and shank. The course is highly variable
  and usually prolonged.
• Gross lesions characteristically, they occur on
  the surface of bones in association with the
  periosteum and near cartilage.
• Tumors often develop at the osteochondral
  junctions of the ribs, inner sternum, pelvis and
  cartilaginous bones of mandible and nares.
• Flat bones of the skull and vertebrae are also
  often affected.
• Hematology the disease is usually aleukemic, but
  occasionally is associated with erythroblastosis.
  Sometimes a heterophilic leukocytosis is present.

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Myloid leukosis (ALV.J)

• It causes predominantly myeloid leukosis
  (Mylocyto-matosis ML) in broiler and commercial
  broiler flocks at 4 weeks of age and older.
• The frequency of tumors varies considerably
  between lines of chickens. It has slow tropism
  for bursal follicle cells, but high tropism for
  cultured blood monocytes.
• In subgroup J Moderate to great enlargement of
  liver, spleen, thymus, gonad and kidney.
  Skeletal Tumor stunting due to its effect on
  pituitary gland hypothyrodisim.
• ALV-J spreads vertically through the embryo and
  horizontally by contact, producing tolerant
  viremic birds and immune birds, respectively. All
  birds of the former class are shedders and
  transmitters of ALV-J to their progeny, as are a
  few birds in the immune class.
• Meat type birds infected soon after hatching
  are particularly prone to becoming tolerant also.
  
• Shedder can be identified by testing vaginal
  swabs and egg albumen for ALV groups-specific
  antigen by ELISA, allowing ALV-J eradication
  protocols to be designed.

monocytes
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Osteopetrosis

• The disease is most commonly seen in birds 8-12
  wk of age or may develop any time after 1 month
  of age.
• It is seen sporadically in the field and more
  often in males than in females.
• Signs
• Long bones of the limbs are most commonly
  affected.
• Jerky gait with uniform or irregular thickening
  of the diaphyseal or metaphyseal regions were
  observed.
• Birds with advanced disease have characteristic
  boot-like shanks. Affected birds are usually
  student and pale due to secondary anemia.
• Gross Lesions
• Visible changes occur in the diaphysis of the
  tibia and/or tarsometatarsus.
• Alterations soon are seen in other long bones
  and bones of the pelvis, shoulder girdle ribs.
• Marrow cavity is narrowed or completely
  obliterated by newly formed bone tissues formed
  thickening (hyperplasia) of periosteum and
  abnormal bone is spongy Anemia.
• Atrophy in bursa, thymus with enlargement of
  liver.
• Hematology The blood picture is ordinarily
  aleukemic and there is often a secondary anemia
  (as a result of reduction of the marrow) with
  relative lymphocytosis.

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Hematological Differential diagnosis between some
forms of ALVs
Lymphoid leukosis Myelocyto-matosis Myelo-blastosis Erythro-blastosis Constituents of the blood
16/55 88/55 Watery blood Plasma
69/1 Thick buffy coat 1/1 Leukocytes
15/44 11/44 Erythrocytes
Immature lymphoblasts or pseudopoded lymphocytes monocytes Myeloblasts 75 of bl. cells Erythroblasts Blood film
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ALSVDiagnosis

• Signs and gross lesions are not indicative
  methods.
• Isolation of the ALSV on ECE or cell culture is
  not easily applied as routine methods.
• A number of biologic assays can be used for the
  detection of endognous and exogenous ALVs as PCR
  to detect DNA.
• Indirect biologic assays such as
• Phenotypic mixing resistance-inducing factor
  (RIF) are used for the detection of ALVs.
• (COFAL), or (ELISA) for ALV (ELISA-ALV),
• The most sensitive procedure for differentiating
  between endogenous and exogenous ALVs is the
  virus isolation and ELISA test.
• The most specific test for detection of antibody
  to ALVs is the virus neutralization (VN) test,
  indirect immunoperoxidase test and ELISA tests.
• For detection of exogenous ALV, samples are
  inoculated on CEFs that are genetically resistant
  to subgroup E ALV. Seven to 9 days later, cell
  lysates are tested for the presence of ALV gs
  antigen by ELISA.

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ALSVPrevention and Control

• I- Immunization No vaccines that protect
  chickens from infection with ALV are available
  commercially.
• II- Eradication depends on breaking the vertical
  transmission of virus from dam to progeny. The
  program is based on the elimination of dams that
  test positive for ALV gs antigen by COFEL, RIF or
  ELISA.
• Sanitation and isolation rearing of susceptible
  chicks is the only practical means available at
  present.
• Ectoparasites should be kept in check at all
  times.
• Live virus vaccines should be prepared from
  leukosis free-eggs.
• (III) Genetic resistance.