This document discusses avian neoplastic diseases, specifically Marek's disease and lymphoid leukosis in chickens. It provides details on the etiology, pathogenesis, clinical signs, pathology, diagnosis and prevention of these two cancers. Marek's disease is caused by a herpes virus and causes tumors in nerves and organs. Lymphoid leukosis is caused by retroviruses and initially causes tumors in the bursa of Fabricius then spreads to other organs like the liver. The document compares the key differences between Marek's disease and lymphoid leukosis.
1. 1
AVIAN DISEASES AND PRODUCTION (VMPA 302)
NEOPLASTIC DISEASES
BY
DR. F. S. UMAR
DEPARTMENT OF VETERINARY PATHOLOGY,
FACULTY OF VETERINARY MEDICINE,
AHMADU BELLO UNIVERSITY, ZARIA
2. AVIAN CANCER
Synonym: Avian leucosis complex
Avian cancer is a group of related and unrelated conditions all showing
neoplastic characters. Some diseased members have known aetiologic
agents, while some others have no known aetiology.
The virus induced tumors are principally of mesodermal origin and are
transmissible.
Many of the virus strains are multipotent i.e. they can sometimes induce
a variety of neoplasms.
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3. • Many virus strains are multipotent i.e. they can sometimes induce a
variety of neoplasms.
• Examples of cancer in poultry are;
(1) Marek’s disease (MD), mainly affecting Chickens, Turkeys and in
Quails.
(2) Lymphoid leucosis (LL) – Mainly in chickens
(3) Osteopetrosis [cancer of bone and is mainly in chickens]
(4) Reticulo-endotheliosis [this disease is mainly in turkey and
chickens]
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4. Some neoplasms originate in specific organs/tissues but spread by
metastasis. Examples include:
1. Sarcoma
2. Nephroplastoma
3. Erythromyeloblastosis
4. Myelocytomatosis
5. Ovarian carcinoma
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5. Marek’s Disease:
Formerly referred to as Neurolymphamatosis. It is a highly infectious disease
caused by herpes virus and is characterized by gross enlargement of the
schiatic nerve and brachial plexus. Also presence of tumors (nodules) on
visceral organs, skin and muscle.
It was 1st described by Prof. Josef Marek, a Hungarian. In 1907 when he
described it, he called it “Range Paralysis”. It was called Neurolymphamatosis
before the name Marek’s was given to it in honour of the man who
described it.
This is the 1st naturally occurring neoplastic disease in any specie to be
controlled by vaccination.
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6. Etiology:
Marek’s disease, caused by Marek’s Disease Virus (MDV)
Marek’s disease virus belongs to the family herpetoviridae and the sub
family Alphaherpatoviridae specifically MDV is designated as gallid
herpes virus-2, which is pathogenic for chickens. It is an enveloped DNA
virus. A linear double stranded DNA smolecule (ds-DNA).
Meleagrid herpes virus-1 is the non-pathogenic herpes virus of turkey
(HVT) which has been used for many decades in vaccine manufacture
to protect chickens.
Although, the domestic chicken is a natural host to MDV, some
infections have been observed in Quails and turkeys.
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7. Transmission/ Spread:
Marek’s disease virus (MDV)
enters into the chicken
through the respiratory
tract.
Feathers, skin and dust are
the major source of MDV
infectious materials and the
basis of horizontal bird-to-
bird transmission in field
conditions
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8. Pathogenesis:
There are two main phases;
Phase 1: Early productive virus infection and replication
causing primarily degenerative changes
Phase 2: Proliferation phase; Establishment of infection: There
is involvement of reticular lymphoid cells.
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9. Clinical Signs
(A). Conventional Clinical form; under field conditions:
- Mortality range is variable but usually between 10 – 20%, affecting
mostly younger chickens.
-The common symptom is paralysis of the wings and legs (brachial and
sciatic nerves affected >> progressive spastic paralysis( i.e. paralysis
accompanied by muscular rigidity).
-Birds rest with one leg stretched forward with the other held behind
commonly referred to as “Hurdle Jumper position”
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10. Clinical signs contd…
(B) Highly Pathogenic Clinical form (VV + MD)
- Mortality ranges from 20 – 50%
-Highly pathogenic MDV can affect matured chicken, ranging in age
from 19 – 21 weeks through horizontal transmission.
-Highly pathogenic marek’s disease virus can persist in infected flock of
adult birds resulting in outbreak in both 1st and 2nd cycle (moulted
hens).
-Other clinical Signs include anorexia, depression, transient paralysis
about 10 days post infection, also ocular infiltration of the virus result
in blindness, distorted iris shape, discolored iris
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13. Various forms of Marek’s disease
Based on clinical manifestation, we have thesefour major
forms;-
Neurologic :- paralysis, drooping wings, extended legs,
torticollis
Ocular : -Blindness, distorted iris shape, discolored iris
Cutaneous : -enlarged feather follicles, leg lesions
Visceral :- Nodular diffuse visceral lymphoid tumors
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14. Pathology:
Gross lesions:
(A) Conventional Marek’s Disease:
(i) Transformation of the hepatocytes to neoplastic ones giving the liver
a grey or white appearance.
(ii) Tumor infiltration of organs may be diffused or nodular
(iii) In some cases, muscles and the skin are involved in tumor
formations
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15. (iv) When the skin is involved as seen in Cutaneous leucosis, tumors
cause feather follicles to be enlarged.
(v) There may be neoplastic enlargement of peripheral nerves and
spinal ganglia, such that the schiatic nerve and brachial plexus loosed
their cross striation.
(vi) In some cases there is pupil irregularity with narrow spotty
depigmentation of the iris making the eye to change color to grey ( grey
eyes).
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16. (B) Highly Pathogenic MD:
These prototype of MD are highly invasive, immunosuppressive,
tumorgenic, causing transformations in target tissues including;-
(i) There is atrophy of lymphoid tissues including thymus and spleen.
(ii) There is splenic necrosis
(iii) There is multifoci tumor formation on thymus, liver, spleen as early
as 5 days post infection.
(iv) The proventriculus is greatly thickened in both the mucosa and
musclaris.
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22. Immunity:
(1) Lymphocytes are responsible for mounting immune responses,
some of which may contribute to protection while others may be
involved in the pathology of the disease (Lymphoma formation and
it is the same cell type that is the primary target (T – lymphocyte for
infection with marek disease virus)
(2) Infection may be lytic resulting in cell death or it may lead to
malignant transformation with both types of infection appearing to be
associated with immunosuppression
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23. Diagnosis
(1) Traditionally, Marek’s disease diagnosis have been based on;
(i) Clinical presentation
(ii) Flocks history
(iii) Gross pathology
(iv) Marek’s disease was a condition of immature flocks and was
characterized with lesions in immature flocks in peripheral nerves. This
was based on assumption that another form of avian cancer called
lymphoid leucosis occurred in matured flocks of breeders and
commercial layers and involved lymphoid tumors in the viscera.
(vi) Laboratory procedures mainly for research purposes includes;
(a) Virus isolations in tissue culture
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24. (b) Antigen demonstration using the fluorescent antibody technique (FAT) on
frozen tissue sections
(c) Antibody demonstration using serum of suspected birds in lab.
Procedures such as; -
- Immunofluorescent test
- Indirect immunofluorescent test
- Virus neutralization
(2) Due to the emergence of highly pathogenic marek’s disease virus (VV +
MVD). These traditionally diagnostic methods have been set aside because
they are unsuitable for differentiation of Marek’s disease and other tumors
such as lymphoid leukosis and reticuloendotheliosis (RE)
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25. (3) Current confirmatory diagnosis of Marek’s disease
Histochemical staining of section of tumors can differentiate
between B and T lymphocyte; Marek’s disease lymphomas are of T –
cell origin, whereas lymphoid leukosis (LL) and reticuloentholusis (RE)
tumors are derived from B – cell lines.
Since Marek’s disease is caused by a herpes virus, while the
differentials LL and RE are caused by retrovirus; advanced
immunologic technique, including immunohistochemistry,
immunocytochemistry and molecular hybridization of DNA are used
to differentiate between these viruses.
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26. Differential Diagnosis of MD
It is based on the clinicopathology of the disease:
1. Nutritional imbalance e.g. Riboflavin deficiency (polyneurosis)
2. Lymphoid leukosis and sarcoma virus groups A,B,C caused by RNA
retrovirus.
3. Reticuloendotheliosis also caused by RNA retrovirus, this sometimes
can induce tumors in peripheral nerves
4. Tuberculosis – due to visceral granulomas
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27. 5. Histomaniasis – Hepatic granuloma
6. New castle disease (Nervous signs)
7. Avian encephalomyelitis – lymphocytic proliferation in the
proventricular wall.
8. Joint infections and injuries e.g. Mycoplasmosis, Colibacillosis or
Staphylococcosis
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28. Lymphoid Leukosis (LL):
Also commonly called Big Liver disease. Primarily a neoplastic transformation of
lymphoid cells of the follicles of the bursa of Fabricius. It is caused by a virus of the
leucosis / sarcoma group and characterized by tumor formation of the bursa of
fabricius with metastasis to other tissues and all abdominal organs.
The neoplastic changes start in bursa and metastasize to the organs, particularly
the liver, spleen and kidneys.
Lymphoid leucosis is a B cell tumor which start in the bursa and before sexual
maturity, may spread to `other organs. Mature or older birds are more affected
than young birds.
Until recently, lymphoid leukosis has been the commonest form of leukosis.
If you observed lymphoid neoplasms in chickens 16 weeks above, in absence of
gross and microscopic damage in peripheral nerves, it is most likely lymphoid
leucosis.
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29. ETIOLOGY
• Lymphoid leukosis is caused by certain members of the leucosis or
sarcoma group of avian retroviruses.
•These viruses are commonly called LL viruses and belong to sub
groups A, B, C, D, E, and J.
• All field strains of LL virus are oncogenic, although some differences
in oncogenicity and replicative ability have been recognized
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30. TRANSMISSION
• Both horizontal and vertical
• Cocks may act only as virus carriers and sources of contact or
venereal infection to other birds.
• Transmission can be reduced or eliminated by strict sanitation.
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32. SUSCEPTIBLE HOSTS
Chickens, some exotic birds.
CLINICAL FINDINGS
• Depression.
• Loss of weight.
• Persistent low mortality.
• Enlargement of abdomen, liver or bursa.
• Many are asymptomatic.
• Chickens with lymphoid leukosis show nonspecific clinical signs including
inappetence, weakness, diarrhea, dehydration, and emaciation.
• The disease occurs in old birds above 16 weeks of age.
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33. PM LESIONS
• Focal or diffuse white or gray neoplastic lesions are seen in the bursa,
liver, spleen and kidneys.
• External tumours may be seen, and the abdomen is enlarged and
feathers are sometimes spotted with urates and bile.
• Tumours may be nodular, miliary or diffuse.
• Bursa are always enlarged and may contain nodular tumours.
• Tumors are smooth, soft and glistening.
• Ecchymotic haemorrhages around the skin follicles of thewing
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34. Diffuse or focal neoplastic
growths of lymphoblasts in
viscera. The neoplastic
changes begin always from
the bursa of Fabricius,
where various-sized
lymphomas are detected
(transverse section through
neo-plastically grown bursa -
fixed preparation)
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35. Severe swelling of the abdomen because of the highly enlarged liver (5X than
normal) with diffuse or nodular neoplastic growths.
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36. A B
A: Spontaneous rupture of the neoplastically grown spleen, leading to extensive loss
of blood.
B: Focal neoplastic lesions in kidneys 36
37. A
B
A: Diffuse and focal tumour lesions in the heart
B: Neoplastically transformed ovary in LL. The replication of the virus occurs in
albumin secreting glands of the oviduct. The transmission of the infection is
performed vertically by egg albumin from one generation to another. 37
38. DIAGNOSIS
• Post mortem lesions and tumors are diagnostic.
• Tumors occur in birds >16 weeks and older.
• In lymphoid leukosis, the lymphoid cells are histologically
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.
• ELISA kits for detection of antibodies to avian leucosis virus
sub groups A, B, and J are available commercially.
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39. DIFFERENTIAL DIAGNOSIS
• Marek’s disease
• Coligranuloma
TREATMENT
• No treatment or vaccines are available.
• Supportive care.
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40. DIFFERENCE BETWEEN MAREKS AND L. LEUKOSIS
FEATURE MAREK’S DISEASE LYMPHOID LEUKOSIS
Virus Herpes virus (ds-DNA) Retro virus( ss-RNA)
Symptoms Usually paralysis or paresis Absent / Non Specific
Incidence Seldom above 5% Usually above 5%
Age 6 Week or older 16 week or above
Cns Or Peripheral Nerve
Enlargement
Affected Not affected
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41. OVARY Not affected Affected
Ocular Lesion Present ( Grey eye) Absent
Feather follicle
epithelium(FFE) affected
Present Absent
Liver tumors Perivascular Focal , diffuse
Cytology of tumors Pleomorphic lymphoid
Cells (small-to-medium
size)
Monomorphic
Lymphoblasts (large
cells)
Category of neoplastic
lymphoid cell
T cells (T-lymphocytes) B cells
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42. Bursa of Fabricius Tumors present Bursa atrophied
Ovary Affected Not Affected
Airborne Infection Present Absent
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43. Other neoplasms of chicken;-
(1) Osteopetrosis:
This is a virus induced hard tissue disease occurring sporadically in the
field in growing birds and is commonly called “marble bone disease”
Recent laboratory transmission experiment have shown that this virus
can produce visceral neoplasms as well. A thickened hard bone cortex
is considered a reliable diagnostic feature.
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44. (2) Erythroblastosis, myeloblastosis and myelocytomatosis:
These neoplasms are seen in growing birds respectively precursors of
Erythrocytes, precursors of granulocytes and the matured granulocytes.
The leukemic neoplasms, erythroblastosis and myeloblastosis results in
hepatomogaly and splenomegaly. Their diagnostic feature is cytologic
and histopathologic, changes in the circulating blood and bone marrow.
Myelocytoma are solid neoplasms that protrude through the hard bone
surrounding the marrow where they originate. The diagnostic feature,
here under histopathology is the presence of masses of matured
granulocytes.
Erythroblastosis is the commonest form among the 3, since the other
two are quite rare.
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45. PREVENTION OF AVIAN CANCER
(1) Genetic Manipulation: Selection of Marek’s disease resistant strain of chicken.
Efficient biosecurity program to eliminate vertical transmission of lymphoid
leucosis.
(2) Immunization to prevent Marek’s disease;
The conventional approach to marek’s disease prevention is by day old
immunization of chickens using bivalent vaccines. (HVT plus SB –1). This is done by
subcutaneous or intramuscular administrations.
(i) Repeat vaccination is at 10 – 21 days once, by the subcutaneous route.
(ii) Most of the vaccines are in the freez dried form. The cell associated virus
vaccines is deep frozen in liquid nitrogen.
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46. (iii) There is an in–ovo injection program for pre-hatching chick embryo
at 18 days of incubation.
(iv) A new vaccine; the type 1 CVI -988 (Ris pens) vaccine is effective in
the prevention of HPMD or VV+MD.
(v) Under field conditions, the type 1 CVI – 988 vaccine is to be
administered only to poultry flocks on farms with history of exposure to
VV + MD, while the conventional HVT plus SB – 1 should be continued
for poultry flocks previously not infected with VV + MD
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47. (3) Chemotherapy (Supportive therapy)
(i) There is no specific curative therapy against any form of avian cancer
and supportive therapy has failed to reverse the pathology caused by
these neoplasms, such as erythroblastosis.
Since some of the neoplasms may be sporadic in occurrence,
Multivitamins administration to apparently healthy pen mates assist
them build greater immunity. Such treatment with antibiotics tend to
reduce further mortality in the flock which may have resulted due to
complications with opportunistic infections.
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