Lymphoid Leukosis management in poultry

13/10/2022

Some chickens have specific genetic resistance to infection with certain subgroups of avian Leukosis virus, although genetic resistance is unlikely to replace the need for reduction or eradication of the virus. Thus far, vaccination for tumour prevention has not been promising. However, recombinant vaccines have been developed that can induce antibodies in breeders to ensure protective maternal antibodies in chicks and these may be useful to assist with eradication programs.

13/10/2022

Eradication of avian leukosis virus from primary breeding stocks is the most effective means to control avian leukosis virus infection and lymphoid leukosis in chickens. Breeder flocks are evaluated for viral shedding by testing for viral antigens in the albumen of eggs with enzyme immunoassays or by biologic assays for infectious virus. Eggs from shedder hens are discarded, so that progeny flocks typically have reduced levels of infection. If raised in small groups, infection-free flocks can be derived with relative ease. These control measures are applied only to primary breeder flocks. Some breeders favor, and have virtually achieved, total eradication, whereas others favor a reduced level of viral infection. Some chickens have specific genetic resistance to infection with certain subgroups of virus. Although genetic cellular resistance is unlikely to replace the need for reduction or eradication of the virus, the cellular receptor gene has recently been cloned, and quick molecular assays for viral susceptibility could be developed. Thus far, vaccination for tumor prevention has not been promising.

13/10/2022

Standard criteria: history and clinical signs, gross pathology, and histopathology
Advanced criteria: immunohistochemistry, standard and quantitative PCR, virus isolation, serology
Because avian leukosis virus is widespread among chickens, virus detection tests, including virus isolation and PCR and the demonstration of antigen or antibody, alone have limited or no value in diagnosing field cases of lymphomas. Gross characteristics of diagnostic significance include the tumorous involvement of the liver, spleen, or bursa in the absence of peripheral nerve lesions. The tumors are found in birds >14 weeks old. Histologically, the lymphoid cells are 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 that demonstrate the characteristic clonal integration of proviral DNA into the tumor cell genome with the associated disruption of the c-myc oncogene. Lymphoid leukosis cannot easily be differentiated from B-cell lymphomas caused by reticuloendotheliosis virus except by virologic assays; however, such tumors probably are extremely rare. PCR primers specific for detection of each subtype of avian leukosis virus have been developed. PCR has been used to detect and characterize avian leukosis virus strains contaminating commercial live virus vaccines of poultry. ELISA kits for detection of antibodies to avian leukosis virus subgroups A, B, and J are available commercially.

13/10/2022

Chickens with lymphoid leukosis have few typical clinical signs. These may include inappetence, weakness, diarrhea, dehydration, and emaciation. Infected chickens become depressed before death. Palpation often reveals an enlarged bursa and sometimes an enlarged liver. Infected birds may not necessarily develop tumors, but they may lay fewer eggs.
Diffuse or nodular lymphoid tumors are common in the liver, spleen, and bursa and are found occasionally in the kidneys, go**ds, and mesentery. Involvement of the bursa has been considered virtually pathognomonic, although bursal lymphomas are also known to be induced by reticuloendotheliosis virus. Sometimes the bursal tumors are small and seen only after careful examination of the mucosal surface of the organ. Usually, no enlargement of peripheral nerves is apparent, although such lesions have been noted after experimental inoculation of subgroup J virus. Microscopically, the tumor cells are uniform, large lymphoblasts. Mitotic figures are frequent.
Lymphoid leukosis, lymphocytic infiltration, muscle
COURTESY OF DR. JEAN SANDER.
Lymphoid leukosis, lymphocytic infiltration, liver
Outbreaks of neoplasms other than lymphoid leukosis such as myelocytomas, hemangiomas, and renal tumors have also been noted in meat-type chickens infected with subgroup J avian leukosis virus. Myelocytomatosis and skeletal myelocytomas may cause protuberances on the head, thorax, and shanks. Myelocytomas may occur in the orbit of the eye, causing hemorrhage and blindness. Hemangiomas may occur in the skin, appearing as “blood blisters,” which may rupture and bleed. Renal tumors may cause paralysis due to pressure on the sciatic nerve. Microscopically, in cases of myelocytomas induced by subgroup J avian leukosis virus, the liver shows a massive intravascular and extravascular accumulation of myeloblasts characterized by the presence of cytoplasmic eosinophilic granules.

Most strains of leukosis/sarcoma viruses also induce nonlymphoid tumors (including sarcomas), erythroblastosis, myeloblastosis, myelocytomas, hemangiomas, nephroblastomas, osteopetrosis, and related neoplasms. The nature of the tumors and their frequency depend on virus strain, chicken strain, age, dose, and route of infection. Occasional outbreaks of predominantly one type of tumor are seen in the field. The Rous sarcoma virus, a member of this group, has been widely studied in the laboratory. Each strain usually causes a predominantly neoplastic disease and can be distinguished on the basis of pathogenicity. Some viruses (eg, Rous sarcoma and erythroblastosis viruses) contain a viral oncogene that enables the virus to induce neoplasms within a short incubation period, but such viruses are rare in the field. Others cannot replicate on their own and require a nondefective helper virus. In recent years, avian leukosis virus infection has been shown to be associated with the so-called “fowl glioma,” characterized by cerebellar hypoplasia and myocarditis.

17/05/2022

In March of 2019, the National Chicken Council petitioned the U.S. Department of Agriculture’s Food Safety and Inspection Service (FSIS) to treat extremely rare lesions suspected to be caused by avian leukosis as trimmable during processing and not a one that requires the whole chicken to be discarded, because it is a localized disease rather than systemic. On July 21, FSIS granted the petition. FSIS must now publish a proposed rule in the Federal Register, followed by a public comment period before the rule becomes final.
Amending the current regulations is supported by scientifically sound rationales, including:
Avian leukosis does not present a food-safety risk
Modern understanding of the avian disease is much more advanced than when FSIS first developed its policy
Leukosis is not a systemic disease
Modern vaccination and breeding programs have all but eliminated avian leukosis
Below are some frequently asked questions and answers about avian leukosis.
What is avian leukosis?
Avian leukosis virus belongs to a family of viruses called “retroviruses.” The virus cannot spread to humans or any other species. Like all retroviruses, the virus is relatively weak and does not survive well outside of the bird. Avian leukosis impacts the bird’s immunity, and the virus can eventually form lesions in the internal organs of the bird such as the liver or spleen.
How often does avian leukosis occur?
According to FSIS data, avian leukosis is a “rare manifestation” in broiler chickens.1 According to the agency’s data from as early as 1984, avian leukosis was present in only 0.017 percent of young chickens slaughtered.2 That number is less than 0.001% today, or one-one thousandth of one percent.
Modern treatment, vaccinations, flock handling practices and biosecurity have effectively eliminated leukosis in commercial broiler and breeder operations. Nearly all birds are vaccinated against the causes of avian leukosis and its prevalence has been effectively eliminated from commercial flocks.
Is avian leukosis a food safety concern? Can it make someone sick?
USDA’s FSIS and other health agencies have recognized avian leukosis “is not transmissible to humans” and “does not present a human health concern,” a fact the agency has acknowledged since at least 1997.3 The viruses that cause leukosis are species-specific and cannot be transmitted to humans. The National Institutes of Health (NIH) has declared that neither virus “is associated with disease in healthy adult humans.”4 Comprehensive literature reviews of the viruses that cause leukosis have also concluded that neither disease presents any apparent risk to public health.5
In the rare occurrence avian leukosis is found on a chicken liver or spleen, are the other parts of the bird, like the breast or wings, affected?
No. In the small chance these lesions occur, they are easily found on the bird’s organs, such as the liver or the spleen, and the organs are discarded. The disease is local and not systemic, meaning it is confined to the organ and does not spread to other parts of the bird.
Considering these facts, NCC is requesting in our petition that the other parts of the bird – e.g. the breast meat, wings, drumsticks, etc. – not be thrown away because they are completely wholesome. In an effort to reduce food waste, we have an ethical obligation to use every part of the bird that is completely safe for human consumption.
Can avian leukosis be transmitted from birds to humans?
There is no scientific evidence to support the claim avian leukosis can be transmitted from birds to humans.
Does this mean USDA inspectors will no longer be inspecting chickens for avian leukosis?
There is and still will be FSIS inspectors on every production line inspecting each carcass after the carcass has been cleaned, inspected and trimmed, if necessary. Company employees are already trained to look for, and eliminate, lesions, bruises etc. on carcasses that are quality issues and pose no food safety concerns. The FSIS inspectors are the final check before the carcasses can move further through the process. By law, a plant cannot operate without FSIS inspectors present and inspecting each carcass before receiving the USDA seal for wholesomeness.

Lymphoid leukosis is a neoplastic disease of poultry caused by avian leukosis virus. The disease is

17/05/2022

Lymphoid leukosis (LL) was eliminated from 3 in**ed lines of White Leghorn chickens that were temporarily kept in isolation. The method of control was based on three elements: 1) From an infected flock we selected hens that produced LL virus-free eggs. Pooled extracts from groups of embryos were tested for vertical virus transmission by the nonproducer cell activation test. 2) Only eggs from dams that did not congenitally shed virus to their embryos were used to produce progeny. The offspring were reared in isolation for 2 months (at which time the age-related resistance against tumor formation had developed sufficiently). 3) The birds were subsequently inoculated im with 10(5) mean tissue culture infective doses of LL viruses of subgroups A and B and transferred to a conventional chicken house. The controlled exposure provided immunity against LL virus infection in a highly infect environment. This procedure resulted in birds a) with no boservable LL, and b) producing LL virus-free eggs. To obtain flocks that had no LL and produced virus-free progeny, the procedure had to be repeated for at least two generations due to the intermittent virus excretion that often occurred.

17/05/2022

Lymphoid leukosis (LL) is virus-induced, lymphoblastic malignancy of chickens that can be congenitally transmitted. Mortality from LL is generally low. Effects of LL virus (LLV) on production and mortality were investigated in approximately 2000 Leghorn pullets in each of two consecutive years. The pullets were from nine strains developed in Ottawa, of which three were unselected control strains and six were strains under selection for up to 27 generations for high egg production and a complex of related commercially important traits. The overall frequency of birds shedding LL virus of gs antigen into eggs (LL-S) was significantly lower in the selected strains (3.9%) than in the control strains (18.5%), indicating that LLV may have negative effects on production and cause elimination of LL-S birds by selection. Such significant effects were indeed detected: the LL-S pullets produced to 497 days of age in 1976 and 1977, respectively, 30 and 25 eggs less per hen-housed than the nonshedders. The LL-S birds matured sexually later, produced smaller eggs at a lower rate, and their eggs had a lower specific gravity, indicating thinner shells. Mortality from all causes to 497 days was significantly higher in LL-S birds (+14.8%) in 1976. In 1977 the increase (+5.5%) did not reach statistical significance. In both years the mortality from LL itself remained very low. In another study, eggs from one of the control strains were incubated and hatched from the dams were 291 and 483 days old. The eggs from LL-S dams had 2.4% lower fertility and 12.4% lower hatchability. The effects on hatchability were more pronounced in the older dams. Since the lower production of LL-S birds results in a lower frequency of such birds in strains selected for high egg production, it is suggested that a part of the difference between the performance of the selected and control strains (delta S) is due to reduction in the frequency of LL-S birds (delta L) rather than due to true genetic gain. In this study, the size of delta L relative to delta S was estimated at 4 to 14% for egg production and 3 to 7% for egg weight. The negative effects of LLV infection on egg production, mortality, hatchability, and genetic gains show the desirability of producing chickens free of LLV infection.

17/05/2022

Fivc groups of genetically susceptible chickens were inoculated at hatching
with lymphoid leukosis virus; four of these were given infectious bursal viruses of varying
virulence at 14 days of age and one group was not inoculated (control). All chickens in the
control group developed evidence of lymphoid leukosis by 180 days. Two groups given
relatively virulent bursal discasc viruses. which destroyed bursal lymphoid cells. did not
develop lymphoid leukosis. Treatment with avirulent vaccines had no visible effect on bursal
morphology and did not significantly alter the incidencc of lymphoid leukosis in two other
groups, although the time of dcvelopment was delayed. Results of our study show that viralinduced destruction of the bursa of Fabricius eliminates the development of lymphoid
Icukosis but that infection without bursal destruction has little effect on lymphoid leukosis.
Lymphoid leukosis, an oncornavirus-induced aleukemic disseminated lymphoma
of chickens, is characterized by malignant transformation of bursa-dependent B
cells. When newly hatched chicks of a genetically susceptible strain are inoculated
at hatching with an oncogenic isolate of lymphoid leukosis virus, transformation of
bursal lymphoid cells occurs when the chicks are 6 to 8 weeks old. By 10 to 16
weeks, transformed follicles are visible in nearly all chickens and metastasis from
the bursa to viscera occurs about the time of sexual maturity at 20 weeks.
The oncogenic effect of lymphoid leukosis virus is accompanied by an interrup
tion of the switch from IgM to IgG, which occurs in B cells of the normal bursa
41. The presence of an intact bursa is obligatory for the B cell transformation
which initiates disease. Surgical bursectomy or testosterone-induced bursal atrophy, when done before the B cell transformation, will destroy the capacity of
lymphoid leukosis virus to induce tumors; thymectomy has no effect.
Infection with virulent infectious bursal virus, which causes severe atrophy of
the bursa 21, suppresses the subsequent development of lymphoid leukosis
When infectious bursal virus is given experimentally, signs of disease begin 48 to
72 hours after inoculation and at 96 hours fever, viremia and inflammation of the
bursa are at their maximum. The causal virus, a distinct nonenveloped icosohedral
60-nanometer RNA-containing virion 17, 8, 111 with no antigenic relationship to
376
Lymphoid Leukosis and Bursa1 Discasc 377. Cumulative death rates of chickens with lymphoid leukosis (dotted lines), times
of death (M). and chickcns that died early from anemia. ascites and bone marrow atrophy
lymphoid leukosis virus, can be identified in lymphocytes and endothelial cells in
the bursa. Lymphoid necrosis, reticuloendothelial hyperplasia and mucous metaplasia of reticuloepithelial cells lead to destruction of the bursa and loss of function
as primary lymphoid organ.
Because infectious bursal disease is an important cause of loss of 3- to 6-weekold chickens and because commercial vaccines are used to control it we wanted to
determine their effect in the suppression of clinical lymphoid leukosis. The
experiment was designed to clarify whether suppression of lymphoid leukosis was
due to bursal lymphoid destruction or to a more finite effect of infectious bursal
virus.
Materials and Methods
The chickcns used wcrc a cross between Regional Poultry Research Laboratory (RPRL)
line 15, males and line 7, females. They wcrc hatched at the RPRL. inoculated with
lymphoid leukosis virus. transported to the National Animal Disease Center and maintained
378 Cheville et nl Atrophic bursa 5 days after inoculation with commercial vaccine. Lymphoid
necrosis. reticuloendothelial hyperplasia and mucous metaplasia of reticuloepithelial cells
(arrow).: Normal bursa 5 days after inoculation with avirulent Vero vaccine. Large
lymphoid folliclcs and intact bursal pads (arrow).
in separate isolation rooms with filtered air supply. Caretakers showered and changed
clothing between pcns. Rous-associated virus- 1 (RAV- 1). known to induce lymphoid
lcukosis. was used. Chicks were inoculated with I x lo2 tissue culture infectious doses of
RAV-I by the intraabdominal route on the day after hatching.
Chickcns that died during the experiment and those that survived to 180 days (the
termination date) were autopsied and the liver, bone marrow and lymphoid organs were
examined histologically. Tissues were fixed in 10% formalin. dehydrated in ethanols and
embedded in paraffin. Sections were stained with hematoxylin and eosin (HE) and periodic
acid-Schiff (PAS).
Five groups of 45 chickens each were given lymphoid leukosis virus at hatching. Four of
these groups received infectious bursal virus when chicks were 14 days old. Group 1 was the
control (no infectious bursal virus); group 2 was given avirulent (vaccine) infectious bursal
virus grown in Vero cell cultures; group 3 was given avirulent (vaccine) infectious bursal
virus grown in chick embryo fibroblasts; group 4 was given dehydrated commercial vaccine
of moderate virulcnce; and group 5 was given virulent field isolate of infectious bursal (table
I). To infect chickens in groups 4 and 5, we placed one drop of viral suspension into the
right eye; to infect groups 2 and 3. 0.4 milliliters of inoculum was injected intramuscularly.
The field strain virulent infectious bursal virus inoculum (group 5) was prepared from
infective bursae that were collected aseptically. ground in a TenBroek grinder with 10
volumes of saline, and centrifuged at low speed to remove debris. The supernatant fluid was
frozen at -70" C and used as stock inoculum 121. The cell culture vaccines (groups 2 and 3)
were prepared by harvesting fluid from infected cell cultures with subsequent lyophilization.
The commercial vaccine (group 4) was purchased as a dehydrated preparation of chicken
embryo origin. An estimate of the effect of each infectious bursal viral inoculum was
obtained by killing five chickens from each group 5 days after inoculation and examining
their bursae histologically. Five chickens from each group were bled at 95 days and serum
titers against infectious bursal virus determincd by a microtiter viral neutralization system
Lymphoid Leukosis and Bursa1 Disease 379: Initial nodular lesion of
lymphoid leukosis within an enlargcd bursal fold.
using constant virus and dilutions of serum IIO]. The virus dose contained 1000 plaque
forming units and sera were serially diluted by two-fold increments.
Results
Bursae from chickens given the field isolate and the virulent vaccine of infectious
bursal virus had marked destruction of the bursal lymphoid follicles no
chickens died of infectious bursal disease. Bursae from control chickens and those
given the two cell-culture vaccines had no visible structural changes
Antibody titers against infectious bursal virus as determined by viral neutralization
tests were: group I (nonvaccinated), all 0; group 2 (Vero vaccine), three were 0,
one was 1 :2 and one was 1 :4; group 3 (CEF vaccine), four were 1 :2, one was 1 :8;
group 4 (commercial vaccine), all 2 1 : 1024; group 5 (field strain), all 2 1 : 1024.
Chickens inoculated with RAV-1 and not subsequently treated developed
evidence of lymphoid leukosis; 38 died of lymphoid leukosis during the experiment
and two had bursal lymphoid tumors at the end of the experiment. The
bursal lesion requisite for the diagnosis of lymphoid leukosis in the chickens
without visceral tumors was the transformation of more individual bursal follicles.
Grossly, the initial lesion could be seen as focal enlargement of one or more bursal
folds. Histologic examination of bursae not affected grossly occasionally
showed transformation of individual follicles. Bursae with transformed
follicles often contained many follicles with necrotic central zones
Chickens given RAV- 1 and avirulent cell culture infectious bursal virus vaccines
(groups 2 and 3) developed lymphoid leukosis although the disease developed
slightly later than in the control group. Although more chickens survived to the
termination date of 180 days, all but one had evidence of bursal follicular
transformation. In contrast, chickens infected with RAV-1 and virulent infectious
bursal virus preparations (groups 4 and 5) did not develop visceral tumors and
only five had evidence of tumor formation in the bursa at 180 days.
Several birds in the five groups died early in the experiment of a syndrome
380 Cheville et a1 Initial lesions of lymphoid leukosis in bursa. Surface elevated by tumorous follicle
that has encroached on adjacent follicles.
characterized by severe anemia, cardiac failure and ascites. The bone marrow of
these birds contained moderate to severe degrees of atrophy. Lymphoid organs,
liver and pancreas appeared normal structurally. This syndrome may represent an
early effect of lymphoid leukosis virus upon the hematopoietic system.
Discussion
The results indicate that bursa1 destruction significantly suppressed lymphoid
leukosis in RAV-1 infected chickens. Infectious bursal viruses that did not destroy
the bursa did not suppress lymphoid leukosis. The effect of infectious bursal virus
is probably the destruction of target lymphoid cells required for malignant
transformation. Alternatively, however, the suppression of an unidentified bursal
humoral factor cannot be excluded as mechanistic.
A transient immunosuppression accompanies the viremic phase of infectious
bursal disease and has been proposed as a factor in the enhancement of other viral
infections. It also is responsible for poor humoral responses to
commercial viral vaccines. It seems unlikely, however, that the transient immunosuppression that accompanies acute infectious bursa1 disease could inhibit lymphoid leukosis development.
The results of this and previous experiments indicate that the low incidence of
lymphoid leukosis in commercial flocks with a high lymphoid leukosis virus viremia

28/04/2022

How do chickens get tumors?
There are two types of mechanism: lymphoid leukosis virus (most common) slowly transforms cells into neoplastic ones and the acutely transforming viruses do the damage faster, all of them using and damaging genes and causing tumours which can include fibrosarcoma, chondroma, endothelioma, haemangioma, nephroblastoma …
Can a chicken have a tumor?
On the basis of this study, it is apparent that hens have a high rate of ovarian tumors, but that such tumors are uncommon in hens less than 2 years of age. Adenocarcinomas with a high degree of morphologic variability are the most common ovarian tumors in hens.
Is lymphoid leukosis contagious?
The virus is not highly contagious compared with other viral agents and is readily inactivated by disinfectants. Transmission can be reduced or eliminated by strict sanitation. After the infection is eradicated, standard disease control and sanitation practices can keep chicken flocks free of the disease.
How is lymphoid leukosis treated?
There is no treatment for Lymphoid Leukosis. Lymphoid Leukosis appears to be controlled best by reduction and eventual eradication of the causative virus, which are rapidly inactivated at ambient temperature and on exposure to most disinfectants.
Why does my chicken have a big lump on its chest?
You know your chicken’s crop is full when it looks like a lump near its breast bone. Bacteria in the crop break down food further into more digestible pieces before moving it into the proventriculus or gizzard.
What are the most common diseases in chickens?
Here are six of the most common health issues chickens face:
Fowl Cholera. Fowl Cholera is a chronic disease caused by Pasteurella Multocida that can affect the joints, wattles, infraohits, sinuses and other tissues.
Coccidiosis.
Avian Influenza.
Fowl Pox.
Newcastle Disease.
Salmonellosis.
What is Marek disease in chickens?
Marek disease is a highly contagious viral disease of poultry characterized by T-cell lymphomas and peripheral nerve enlargement. Standard criteria used for diagnosis include history, clinical signs, gross necropsy, and histopathology. Although no treatment is available, current vaccines are highly protective.
How do you treat crop impaction in chickens?
Impacted crop can be treated by lubricating the crop/digestive tract with vegetable oil in an eyedropper through the mouth and massaging the crop to try and break up the blockage, or in extreme cases actually slitting the crop open with a scalpel and removing the blockage.
How can you tell if chicken is sour crop?
Symptoms. The crop feels like a balloon which has filled with water. Gentle pressure applied to the crop when picking the hen up may cause fluid to spill out from her beak. Classic sour crop has a foul smell and the fluid which is voided is often brown, although this is not always the case.
What are the symptoms of coccidiosis in chickens?
Outward signs of coccidiosis in chickens include droopiness and listlessness, loss of appetite, loss of yellow color in shanks, pale combs and wattles, ruffled, unthrifty feathers, huddling or acting chilled, blood or mucus in the f***s, diarrhea, dehydration, and even death.
How do you tell if a chicken has a disease?
Common signs of disease in poultry
feather loss (unless birds are going through a natural moult)
general inactivity.
discharges.
abnormal droppings.
dull and/or closed eyes.
ruffled feathers.
drooped wings.
sitting on haunches or lying down.
What kind of tumor does a chicken have?
It is not uncommon for some chickens to develop tumors. A tumor is an abnormal growth of tissue, a swelling that appears on the outside or inside part of the chicken’s body. Usually tumors do not appear infected or inflamed.
Are there any cases of ovarian cancer in chickens?
Case 1: Ovarian adenocarcinoma in a Chicken Ovarian adenocarcinoma was detected in a 3-year-old hen from a backyard flock. The hen had been declining in general health. The hen had very depleted skeletal muscle stores and no body fat.
Can a chicken get Lymphoid leukosis and die?
Tumors are found most often in meat type birds but the Lymphoid Leukosis infection exists in almost all chicken flocks “The infection is known to exist in virtually all chicken flocks except for some SPF flocks from which it has been eradicated. Tumor mortality commonly accounts for ~1%–2% of birds, with occasional losses of ≥20%.”
Which is the most common leukosis in chickens?
Under natural conditions, lymphoid leukosis has been the most common form of the leukosis/sarcoma group of diseases seen in chicken flocks, although in the 1990s myeloid leukosis become prevalent in meat-type chickens.

20/09/2021

A complex of viral diseases with various manifestations such as lymphoid leukosis, myeloblastosis (see Sero-type J), erythroblastosis, osteopetrosis, myxosarcomas, fibrosarcomas, other tumours. It affects chickens worldwide with susceptibility varying considerably among different strains and types of stock - egg layers are generally more susceptible to lymphoid leukosis.
Morbidity is low but mortality high. Mortality tends to be chronically higher than normal for a prolonged period. Egg production is somewhat reduced. There may be increased susceptibility to other infectious diseases due to damage to the immune system. Vertical transmission is most important by infection of the egg white in infected breeders (who are long-term carriers), lateral transmission is poor but infection may occur by the faecal-oral route, especially in young birds. In lymphoid leukosis the incubation period is about 4-6 months; it may be as short as 6 weeks for some of the other manifestations. The causative viruses are rapidly inactivated at ambient temperature and on exposure to most disinfectants.
Signs
Depression.
Emaciation.
Loss of weight.
Persistent low mortality.
Enlargement of abdomen, liver or bursa.
Many are asymptomatic.
Post-mortem lesions
Focal grey to white tumours, initially in the bursa, then liver, spleen, kidney etc. Liver may be very large.
Microscopic - cells lymphoplastic
Diagnosis
History, age, lesions, cytology. Differentiate from Marek's disease, coligranuloma.
Treatment
None.
Prevention
Good hygiene, all-in/all-out production, control arthropods, eradication - checking of antigen in the albumen is a basis for eradication (see Sero-type J for details).