- Host Animals
- Hosts/Species Affected
- Systems Affected
- Distribution Table
- List of Symptoms/Signs
- Disease Course
- Impact: Economic
- Zoonoses and Food Safety
- Disease Treatment
- Prevention and Control
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- avian leukosis
International Common Names
- English: avian leukosis, sarcoma, virus infection
Pathogen/sTop of page
OverviewTop of page
The term 'avian leukosis' embraces several different leukaemia-like proliferative diseases of the haemopoietic system caused by avian leukosis viruses (ALVs). The components of the haemopoietic system that may undergo neoplastic change include the lymphopoietic (lymphocytic), the erythropoietic (red cell), and the myelopoietic (myelocytic) systems.
Host AnimalsTop of page
|Animal name||Context||Life stage||System|
|Gallus gallus domesticus (chickens)||Domesticated host||Poultry: Day-old chick|Poultry/Young poultry|Poultry/Mature female|Poultry/Cockerel|Poultry/Mature male|
Hosts/Species AffectedTop of page
Various species of birds are susceptible to infection by ALVs, although clinical disease is mainly encountered in chickens. Domestic chickens are infected by ALV subgroups, A, B, C, D, E and J. The F, G, H and I subgroups of ALV are allocated to endogenous viruses found in ring-necked and golden pheasants, grey partridge and Gambel’s quail, respectively (Payne, 1992).
Systems AffectedTop of page
multisystemic diseases of poultry
DistributionTop of page
ALVs are almost ubiquitous in commercial chickens on a worldwide basis, although many primary egg-type and meat-type breeding companies institute ALV eradication schemes. Among the exogenous ALVs, the subgroup A viruses occur frequently and subgroup B viruses more rarely. Nevertheless, the incidence of neoplasms, mainly lymphoid leukosis, in infected flocks is usually less than 2%, although losses of up to 20% can occur. Subgroup C and D viruses have not been widely recognised in the field. Endogenous subgroup E viral loci are present in virtually all stock, and may be expressed as exogenous viruses in some strains of chickens. Subgroup J ALV is widely distributed globally in meat-type chickens, and neoplastic losses, mainly from myeloid leukosis, vary up to around 50% (Payne, 1998).
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.Last updated: 10 Jan 2020
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Central African Republic||Absent, No presence record(s)|
|Congo, Democratic Republic of the||Absent, No presence record(s)|
|Djibouti||Absent, No presence record(s)|
|Eritrea||Absent, No presence record(s)|
|Madagascar||Absent, No presence record(s)|
|Mauritius||Absent, No presence record(s)|
|Seychelles||Absent, No presence record(s)|
|Sudan||Absent, No presence record(s)|
|Tunisia||Absent, No presence record(s)|
|Zambia||Absent, No presence record(s)|
|Bahrain||Absent, No presence record(s)|
|Hong Kong||Absent, No presence record(s)|
|Iran||Absent, No presence record(s)|
|Kazakhstan||Absent, No presence record(s)|
|-Peninsular Malaysia||Absent, No presence record(s)|
|North Korea||Absent, No presence record(s)|
|Oman||Absent, No presence record(s)|
|Syria||Absent, No presence record(s)|
|Vietnam||Present||CAB Abstracts Data Mining|
|Czechia||Absent, No presence record(s)|
|Estonia||Absent, No presence record(s)|
|Isle of Man||Absent, No presence record(s)|
|Jersey||Absent, No presence record(s)|
|Latvia||Absent, No presence record(s)|
|Liechtenstein||Absent, No presence record(s)|
|Lithuania||Absent, No presence record(s)|
|North Macedonia||Absent, No presence record(s)|
|Portugal||Absent, No presence record(s)|
|Serbia and Montenegro||Absent, No presence record(s)|
|Slovenia||Absent, No presence record(s)|
|Bermuda||Absent, No presence record(s)|
|British Virgin Islands||Absent, No presence record(s)|
|Cayman Islands||Absent, No presence record(s)|
|Curaçao||Absent, No presence record(s)|
|Dominica||Absent, No presence record(s)|
|Guatemala||Absent, No presence record(s)|
|Haiti||Absent, No presence record(s)|
|Honduras||Absent, No presence record(s)|
|Saint Kitts and Nevis||Absent, No presence record(s)|
|Saint Vincent and the Grenadines||Absent, No presence record(s)|
|Trinidad and Tobago||Absent, No presence record(s)|
|Vanuatu||Absent, No presence record(s)|
|Ecuador||Absent, No presence record(s)|
|Falkland Islands||Absent, No presence record(s)|
|Guyana||Absent, No presence record(s)|
PathologyTop of page
This is a common form of leukosis and occurs in chickens from about 4 months of age. Gross pathological changes include enlargement of the liver with miliary, diffuse or nodular tumour foci, and nodular tumours in the bursa of Fabricius and other organs. Microscopically the lesions consist of coalescing foci of uniformly immature lymphoid cells (lymphoblasts). The tumour cells are B-cell derived, originating in the bursa of Fabricius that later metastasise to other organs.
This form (also termed erythroblastosis) is an uncommon, usually sporadic, tumour occurring mainly in adult chickens and occasionally in young (from 5-week-old) birds. The liver and spleen, and sometimes the kidneys, are diffusely enlarged and often of bright cherry-red colour. The bone marrow is bright red with a liquid consistency. Affected birds are often anaemic, with muscle and sometimes abdominal haemorrhages from a ruptured liver. The disease is an intravascular erythroblastic leukaemia. Microscopically, the liver shows intrasinusoidal accumulations of rather uniform, round, erythroblasts, the spleen shows accumulations of erythroblasts in the red pulp, and the bone marrow shows enlarged haemopoietic sinusoids filled with erythroblasts. There is an erythroblastic leukaemia.
This occurs in two, often overlapping, forms: myeloblastic myeloid leukosis (myeloblastosis) and myelocytic myeloid leukosis (myelocytomatosis). Before the advent of subgroup J ALV, myeloblastic myeloid leukosis was mainly a sporadic disease of adult chickens. In this classic form the liver and spleen are greatly enlarged and the liver frequently has a yellowish-grey granular (‘Morocco leather’) appearance. The bone marrow is firm and reddish-grey in colour. Microscopically the liver shows intravascular, sinusoidal, accumulations of immature myeloid cells (myeloblasts and promyelocytes), and extravascular accumulations and perivascular cuffing with these cells. The red pulp of the spleen is infiltrated by myeloid tumour cells, as are the extrasinusoidal myelopoietic areas in the bone marrow. There is a marked myeloid cell leukaemia. Before subgroup J ALV appeared, myelocytic myeloid leukosis occurred mainly in young chickens. In this form, yellowish-white myelocytomas are present in the skeletal tissues and, microscopically, tumour comprises well-differentiated myelocytes.
Myeloid leukosis caused by subgroup J ALV shows features of both myeloblastic and myelocytic forms. The disease occurs mainly in adult broiler breeders, and sometimes in young breeders and broilers. Skeletal tumours such as those seen in the head, ribs, vertebrae, and inner sternum are commonly observed in the infected birds. Lesions can also occur in soft tissues such as the liver, spleen, ovary or thymus. Microscopically, the tumour cells are usually well-differentiated myelocytes, but tumours of more immature myeloid cells occur, sometimes in the same bird.
A variety of solid tumours can be caused by ALV, including fibrosarcoma, chondroma, haemangioma, histiocytic sarcoma, mesothelioma, myxoma, nephroblastoma, osteoma, and the proliferative bone disorder, osteopetrosis, characterised by thickening of the long bones.
DiagnosisTop of page
Both pathological and virological methods of diagnosis are important for making the correct diagnosis of ALV infection. Although the gross appearance of the tumour can provide indications of the nature of a neoplasm, histopathological diagnosis is essential for accurate diagnosis. The most useful tissues to collect are liver, spleen, bursa of Fabricius, bone marrow and other gross tumours.
The following techniques are developed for the specific virological diagnosis of ALV infection.
ALV may be isolated from materials from individual birds as a means of detecting the presence of the infection in the bird or flock. Materials commonly used for isolation include serum, buffy coat cells, and tumour tissue, and for certain purposes, cloacal or vaginal swabs, egg albumen, embryos and meconium (Fadly and Witter, 1998). These are inoculated into C/E chicken embryo fibroblasts (CEFs) and tested for the presence of ALV p27 gs-antigen in an antigen ELISA test. The C/E cells used for this assay will support growth of ALVs of the known exogenous subgroups A, B, C, D and J, but exclude subgroup E ALV of endogenous origin. Most ALV isolated from the field are slowly transforming viruses that lack viral oncogenes. Acutely transforming viruses inducing rapid tumours can be identified by in vitro transformation on bone marrow or blood monocyte cultures.
Characterisation of ALV subgroups
ALV isolates obtained from the CEF cultures can be grouped into different ALV subgroups using the following assays.
- Viral interference assays. This assay tests the ability of an isolate to interfere with focus formation in C/E CEF cultures by Rous sarcoma virus (RSV) of known subgroup.
- Virus neutralisation assays, in which an isolate is placed in a subgroup according to its susceptibility to neutralisation by chicken antisera with known subgroup neutralising activity. The isolate, or its RSV pseudotype, is exposed to antiserum and then examined for growth, or focus formation, respectively, in C/E CEF cultures.
- Host range assays, in which an isolate or its RSV pseudotype is placed in a subgroup according to its ability to grow in, or transform, respectively, CEFs of varying ALV subgroup susceptibility phenotypes. This method relies on the availability of CEF phenotypes that exclude certain ALV subgroups. It should be mentioned that CEFs that exclude subgroup J have not been found occurring naturally, although a C/J CEF line by expressing the ALV-J env has been developed.
- Polymerase chain reaction (PCR) assays specific for various ALV subgroups have been developed. These tests are sensitive, rapid, and may be used to detect ALV proviral sequences in tumour material or cultured CEFs. By use of a reverse transcription step (RT-PCR) the viral RNA in the infectious virus can also be detected.
Detection of ALV p27 group specific-antigen
ALVs of all subgroups share a common p27 group specific (gs)-antigen, which may be detected by an antigen ELISA test. This test is commercially available, relatively cheap, rapid, and can be used on a large scale for detecting ALV in vaginal or cloacal swabs of chickens that shed ALV and in albumen of eggs from shedder hens. This test is used particularly in ALV eradication programmes, and for detecting ALV in cultured CEF. This test lacks subgroup specificity and does not discriminate between exogenous and endogenous ALV. Careful selection of the cut-off point between 'negative' and 'positive' results is needed to discriminate between exogenous and endogenous virus using this test.
Detection of ALV antibodies
Detection of antibodies against ALV is used in flock surveillance to detect presence or absence of infection by exogenous ALV, and to identify particular classes of birds in epidemiological studies and ALV eradication programmes. The most common tests used for the detection of ALV antibodies are the virus neutralisation and antibody ELISA tests.
List of Symptoms/SignsTop of page
|Digestive Signs / Abdominal distention||Poultry:Not known||Sign|
|Digestive Signs / Ascites, fluid abdomen||Poultry:Not known||Sign|
|General Signs / Increased mortality in flocks of birds||Poultry:Not known|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Poultry:Not known||Sign|
|General Signs / Sudden death, found dead||Poultry:Not known||Sign|
|General Signs / Swelling skin or subcutaneous, mass, lump, nodule||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Poultry:Not known||Sign|
|General Signs / Weight loss||Poultry:Not known||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Poultry:Not known||Sign|
|Reproductive Signs / Decreased hatchability of eggs||Poultry:Embryo||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Poultry:Not known||Sign|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Poultry:Not known||Sign|
|Skin / Integumentary Signs / Ruffled, ruffling of the feathers||Poultry:Not known||Sign|
Disease CourseTop of page
The incubation period from infection to the development of the disease is usually 4 months or more. In lymphoid leukosis, the target cells for neoplastic transformation are in the bursa of Fabricius. At variable periods after infection, a focal preneoplastic hyperplasia can be observed. Although many follicles are sometimes affected, the majority will regress and only a few, where cellular oncogenes are activated, will continue to grow, giving rise to development of nodular bursal tumours that are visible from 14 weeks of age. Neoplastic lymphoid cells metastasise from the bursa into other organs such as the liver and spleen resulting in mortality. Erythroblastosis also might have a similar course except that the disease starts from the bone marrow and that the leukaemia is present from the outset.
EpidemiologyTop of page
In the infected flocks, exogenous ALV can spread both by vertical transmission from the infected hens to the progeny and by horizontal transmission by direct or indirect contact between birds (Payne and Fadly, 1997). Vertical (congenital or egg) transmission is important in transmitting the infection from one generation to the next, and in providing a source of contact infection to other chicks. ALV present in the magnum of the oviduct of the hen passes into the egg albumen and into the chick embryo during incubation. Infected males do not pass the infection to their progeny, although the virus present in the semen can infect hens venereally. Horizontal transmission, in which ALV spreads from bird to bird by direct contact or indirectly by exposure to virus in the environment, is responsible for the high incidence of infection in flocks. Sources of virus from infected birds include faeces, saliva and desquamated skin. Congenitally infected chicks are an important source of infection in the hatchery and during the brooding period, and meconium and faeces from congenitally infected chicks contain high concentrations of ALV. Routes of infection are oculonasal, oral, respiratory and skin.
The infective status of chickens in an ALV-infected flock can be grouped according to whether or not they have viraemia (V+ or V-), serum antibodies (A+ or A-), or shed ALV to their cloaca or egg albumen (S+ or S-). On this basis, the birds could be grouped into different classes as follows:
- Tolerant viraemic, antibody-negative, shedders (V+A-S+). These birds arise primarily because of vertical (congenital) infection from the dam, and they in turn produce V+A-S+ progeny. They shed large amounts of virus and group-specific antigen (gsa) into the egg albumen, embryos and chick meconium. V+A-S+ birds are most prone to develop tumours.
- Non-viraemic, antibody-positive, non-shedders (V-A+S-) and shedders (V-A+S+). Birds that acquire their infection by contact after hatching are most likely to develop an immune infection. They are likely to constitute the majority of a flock. They are usually non-shedders, which do not produce infected progeny, but some may be shedders, and produce, intermittently, infected chicks. These birds are less likely to develop tumours.
- Non-viraemic, antibody-negative, non-shedders (V-A-S-). Birds of this class are either not yet infected, or are genetically resistant to infection.
- Viraemic, antibody-positive birds (V+A+). A small class of birds with both viraemia and antibodies may be found. These birds are thought to be seroconverting from a transient viraemic state to an immune (V-A+) state and may or may not shed virus.
Impact: EconomicTop of page
Economic losses from leukosis/sarcoma groups of diseases mainly come from subclinical infection that leads to a depressive effect on different performance traits such as egg production, egg size, fertility, hatchability and growth rate. Losses also could result from increased mortality from tumours that usually occurs at 20-36 weeks of age. The worldwide spread of the newly emergent subgroup J strain of ALV (Venugopal, 1999) and associated mortality during the 1990s has placed this infection among diseases of serious concern.
Zoonoses and Food SafetyTop of page
There is no firm evidence that ALV presents any health risk to humans although the possibility of this has not been definitely excluded. It is known that certain strains of the related Rous sarcoma virus, particularly of subgroup D, can infect and transform mammalian cells, including human cells, in vitro, and that they can induce sarcomas and other tumours in vivo in mammals, including primates. However, in spite of exposure of humans to ALV from live poultry, poultry meat, and eggs, no conclusive epidemiological or other evidence has been adduced of any risk of cancer. Also, exposure of man to exogenous ALV present at one time as a contaminant of live vaccines such as yellow fever and measles was not associated with a recognised hazard. Antibodies to ALV have been detected in poultry workers and others but these may result from antigenic exposure rather than being due to ALV replication in humans. However, recently low levels of reverse transcriptase activity found in live human vaccines (measles, mumps, yellow fever) grown in specific-pathogen free (SPF) avian cells have caused some concerns (Weissmahr et al., 1997). These studies revealed the presence of RNA of endogenous retrovirus origin in the vaccines, but no evidence of infectious virus or EAV sequences have been observed in vaccine recipients.
Disease TreatmentTop of page
There is no specific treatment against ALV infections and the most efficient method of control is the eradication of infected stock.
Prevention and ControlTop of page
Eradication of exogenous ALV from flocks
This depends on breaking the vertical transmission cycle of virus from dam to progeny and prevention of re-infection of the progeny and involves the identification and elimination of hens that shed ALV. These hens belonging to the infective classes V+A-S+ and V-A+S+ are identified by testing their cloacal or vaginal swabs, or albumen from their eggs. The test procedures carried out at different ages and all positives are eliminated to ensure that only clean birds are allowed to continue in the flocks (Payne and Venugopal, 2000). Hatched chicks are reared in isolation in small groups and tested for viraemia and ALV antibodies from about 8 weeks of age to verify freedom from infection.
Good hygiene and biosecurity are very important adjuncts to disease control, particularly for leukosis for which there are no vaccines and where commercial flocks free from infection are at risk from re-infection. Good general farm management procedures include isolation of premises, all-in all-out management, cleaning and disinfecting of premises between crops, use of new litter, safe disposal of old litter, and site security. Hatchery hygiene is of equal importance. ALV is a fragile virus outside the bird, with a half-life of only a few hours at room temperatures, and is susceptible to all common disinfectants.
Immunization and Vaccines
Relatively little research has been carried out on vaccine development because it is believed that they would not be effective against a vertically transmitted virus which induces immunological tolerance. However, the propensity of subgroup J ALV especially to induce tolerant rather than immune infections following early contact infection has stimulated interest in developing vaccines to protect chicks against early exposure to ALV-J.
Selection for genetic resistance
Two main types of genetic resistance to leukosis have been recognised: genetic resistance to ALV infection and genetic resistance to development of leukotic tumours. Resistance to infection depends on the lack of specific ALV receptors on the cell membrane, which interact with viral envelope glycoprotein and allow infection to occur. The presence or absence of these receptors is under simple genetic control (Payne, 1985). Three autosomal loci, tva, tvb and tvc, with dominant susceptibility genes encoding the presence of virus receptors and recessive resistance genes encoding their absence, control susceptibility to infection by ALV of subgroups A, B and D, and C, respectively. Poultry breeders can artificially select for the presence of the resistance genes, ar and br, at the tva and tvb loci, and thus develop strains of chickens resistant to infection by the common A and B subgroup ALV.
ReferencesTop of page
Fadly AM; Witter RL, 1998. Oncornaviruses: leukosis/sarcoma and reticuloendotheliosis. In: Glisson JR, Jackwood DJ, Pearson JE, Reed WM, Swayne DE, eds. A Laboratory Manual for the Isolation and Identification of Avian Pathogens. Kennett Square, PA, USA: American Association of Avian Pathologists, 185-196.
OIE Handistatus, 2002. World Animal Health Publication and Handistatus II (dataset for 2001). Paris, France: Office International des Epizooties.
OIE Handistatus, 2003. World Animal Health Publication and Handistatus II (dataset for 2002). Paris, France: Office International des Epizooties.
OIE Handistatus, 2004. World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties.
OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.
Payne LN, 1985. Genetics of cell receptors for avian retroviruses. Poultry genetics and breeding. Proceedings of the 18th Poultry Science Symposium, in association with the 25th British Poultry Breeders Round Table, 1983., 1-16; [Poultry Science Symposium 18]; 103 ref.
Payne LN, 1992. Biology of avian retroviruses. In: Levy JA, ed. The Retroviridae, Vol. 1. New York, USA: Plenum Press, 299-404.
Payne LN, 1998. HPRS-103: a retrovirus strikes back. The emergence of subgroup J avian leukosis virus. Avian Pathology, 27(Supp 1):S36-S45; 35 ref.
Payne LN; Fadly AM, 1997. Leukosis/sarcoma group. In: Calnek BW, ed. Diseases of Poultry. Ames, USA: Iowa State University Press, 416-466.
Payne LN; Venugopal K, 2000. Neoplastic diseases: Marek's disease, avian leukosis and reticuloendotheliosis. In: Diseases of Poultry: World Trade and Public Health Implications. Office International Des Epizooties (OIE) Scientific and Technical Review, 19(2):544-564.
Venugopal K, 1999. Avian leukosis virus subgroup J: a rapidly evolving group of oncogenic retroviruses. Research in Veterinary Science, 67(2):113-119; 32 ref.
Weissmahr RN; Schupbach J; Boni J, 1997. Reverse transcriptase activity in chicken embryo fibroblast culture supernatants is associated with particles containing endogenous avian retrovirus EAV-0 RNA. Journal of Virology, 71:3005-3012.
OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (dataset for 2004)., Paris, France: Office International des Epizooties.
Distribution MapsTop of page
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CABI Summary Records
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