A Brief Guide To

Broilers & Breeders

Diseases
Broiler Breeder Diseases - A Review.
Having a reliable supply of healthy day-old broiler chicks is fundamental to the operation
of any broiler enterprise. Accomplishing this goal depends on healthy breeders, i.e., no
breeders = no eggs = no chicks. Being chickens, broiler breeders are susceptible to the
same diseases as broilers, layers, and other types of chickens. Examples of diseases
shared between broilers and broiler breeders, based on our diagnostic accessions, are
coccidiosis and infectious laryngotracheitis.

However, most diseases that affect broiler breeders tend to differ from those affecting
other types of chickens because of differences in genetics, feeding, husbandry,
environment, and management. Mortality and decreased production frequently can
be attributed to non-infectious diseases or diseases of the reproductive system.

Collectively, mortality tends to be highest in the early lay period between onset and
peak egg production and due to noninfectious diseases . Often breeder diseases are
not well understood or documented and they tend to be complex, involving many
factors. A thorough and careful diagnostic investigation is essential in identifying health
problems in broiler breeders. In this presentation, selected diseases currently affecting
broiler breeders will be reviewed including enterococcal spondylitis, staphylococcosis,
impaired mobility (“calcium tetany”), cloacitis, feather pecking, avian proliferative
pulmonary disease, avian hepatitis E virus infection, and sporadic lymphoid leukosis.

Introduction

While broiler breeders are chickens, and they are susceptible to the same diseases that
affect other chickens (broilers, layers, purebred, small flock, etc.), they tend to have
specific diseases with only a few in common with those of other types of chickens.
Exceptions, based on our diagnostic accessions, are coccidiosis and infectious
laryngotracheitis, which are diseases that have occurred frequently in both commercial
broilers and broiler breeders. Having healthy broiler breeders is critical to the economy
of any broiler company. Unfortunately, diseases of breeders are often poorly understood
and not well documented. Frequently they are non-infectious or involve the reproductive
system, and are multifactorial involving the interplay of genetics, environment, nutrition,
husbandry, and management. Diseases that affect broiler breeders are listed in Table 1.
Obtaining an accurate diagnosis can be challenging, requiring a thorough
understanding of flock history, evaluation of the flock environment, and detailed
necropsy and sampling. Cumulative mortality, especially in males, can be high.

There are several reasons why diseases specifically affect broiler breeders. In contrast
to broilers, broiler breeders have a relatively long production cycle that averages around
65 weeks; there is more opportunity for problems to develop. The "wear and tear" of
breeding and continuous production of fertile eggs also takes its toll on the birds. Having
been highly selected for rapid growth and efficient feed utilization is a double-edged
sword. While the economic traits are desirable, controlling growth of breeders is
essential for their health and reproductive performance. When males are overrestricted,
losses due to starvation occur in the more subservient birds and there may be
inadequate development of both roosters and hens during the pullet period that does
not support their reproductive potential throughout the entire laying period. Losses in
males due to trauma, scavenging in litter and on carcasses, and litter impaction (Roza
et al., 2006) are also possible as a result of restricted feeding. Pullets may engorge
themselves to the point that the hard distended crop compresses the trachea,
sometimes to the point of suffocation. On the other hand, over-conditioned birds that
become too heavy are poor breeders and the females develop a host of disease
problems including early ovarian regression due to super-ovulation, salpingoperitonitis,
prolapse of the cloaca and vagina, and decreased egg production (Chen et al., 2006).
Poor air quality in the pullet or breeder house leads to chronic, obstructive pulmonary
disease from inhaled foreign material that is characterized by multifocal granulomatous
pneumonitis and epithelial proliferation. Breeders are given numerous vaccines to
protect against mortality, egg production drops, and provide high maternal immunity to
chicks, but if the birds are not handled and vaccinated properly, serious losses can
occur. Trauma can result from handling, entrapment in slats or equipment, or high slat
height. Nutritional diseases are possible because of the demands for egg production or
incorrect diets.

In this presentation, selected broiler breeder diseases that are currently affecting the
broiler industry will be briefly reviewed including enterococcal spondylitis,
staphylococcosis, impaired mobility ("calcium tetany"), cloacitis, feather pecking, avian
proliferative pulmonary disease, avian hepatitis E virus infection, and sporadic lymphoid
leukosis.

Disease Diagnosis

History. Identifying health problems in broiler breeders requires a thorough and

complete investigation that starts by getting a good history. Often carefully
understanding the problem shortens the time to a solution. This includes determining
what happened in the pullet house and, if multiple breeding flocks came from a single
pullet farm, how each of those flocks are doing. When investigating a problem of excess
mortality the following information is needed:

1. Strain of broiler (hens and roosters if different)

2. Flock age

3. Flock average body weight relative to breed standard

4. Egg production relative to breed standard

5. Is mortality affecting roosters/hens/or both?

6. Mortality percent
7. Mortality location

Diseases in which mortality is found only in the scratch area include: rooster kill / rooster
aggression and impaired mobility due to ruptured tendons, fractures of femur or pelvis,
osteoporosis, or calcium tetany. When birds are found in either the nest boxes or on the
slats, possible causes of mortality include: reproductive diseases (internal laying,
oviduct impaction, yolk peritonitis or infectious salpingoperitonitis, or cloacal and vaginal
prolapses), choke due to crop impaction, calcium tetany (hypocalcemia), sudden death
syndrome (hypokalemia or hypophosphatemia), obesity (ketosis, acetonemia ,"fat hen
syndrome") or physical injury from nests, feeders, or slats. Mortality found in any
location may indicate fowl cholera or hyperthermia (Powell, 2004).

Site Evaluation. The cause of a disease or factors contributing to the disease, often can
be identified by evaluating the environment. What is the overall condition of the housing
and equipment? Damaged or missing slats lead to entrapment, broken legs, and other
trauma. Ruptured tendons and fractures may result from slats being too high. Are birds
under the slats because the slats are not secure? Is the manure level close to the slats?
Rodents can attack the hens while they rest on the slats if the manure level is high
enough for them to reach the birds. What is the arrangement of male and female feed
lines and water lines? Is there adequate feeder and water space? Do the feeder grills
need repair to prevent trauma and possible entrapment? What is the condition of the
litter and are feathers present or have they all been eaten? Is air quality and
temperature good? What is the overall appearance of the flock? Are the birds well
socialized or are they flighty? What is the level of breeding activity? Are the males
interested in the hens and the hens receptive to being bred? Are nest boxes and egg
belts in good repair and clean? Is the lighting adequate and uniform? High lighting
predisposes to vent persecution (cannibalism) while uneven lighting contributes to
excess floor eggs. Finding decomposing dead birds on the slats or in the litter indicates
the flock is not being monitored adequately and a clear indication of poor management.

Check egg production records to see how they relate to breed standard. A common
finding is to bring pullets into production too early. While the early, high peak looks good
on the production graph, the hens tend to super-ovulate resulting in increased abnormal
(unsettable) eggs, early ovarian regression, premature molting, and metabolic disorders
including myopathy and calcium tetany. The best egg record is the one that stays on, or
just above, the recommended line for the breed standard. Check the eggs. They should
have clean shells - no blood streaks or significant fecal material, normal ovoid shape,
good pigmentation, and shells that are not wrinkled, chalky, thin, or brittle. Break out a
few eggs to check for fertility and internal egg quality. Next evaluate the egg collection
area and egg storage room. Are they clean and free of trash and junk? Is the
temperature and humidity in the egg room correct? Lastly, what are the biosecurity
measures and how well are they working? Check bait stations and areas surrounding
the house for evidence of rodents or rodent activity.

There is no substitute for a site visit. Interviews about conditions on the farm rarely
match what one actually finds.
Necropsy. At necropsy, a thorough examination is necessary with particular attention to
the following:

1. Body weight of mortality. Body weight of mortality is underlined because of its

importance. How body weights of birds that die compare with those of the flock average
can provide useful information about the disease affecting the flock and what may have
caused it. Birds that die suddenly or after a short illness will weigh the same as those in
the flock, whereas sick birds rapidly lose weight as the duration of illness progresses.

2. Body condition determined by the amount of breast muscle. A scale of 1 - 5 is

commonly used with 1 denoting birds with severe muscle atrophy and 5 for birds that
are obese. Healthy hens score 4 while males score 3.

3. Comb and wattles indicate production status, hydration, and cardiovascular function.

4. Footpads and hock joint swelling indicate inflammation that should be aseptically
sampled and cultured for bacteria, mycoplasmas, or viruses. Wing tips of lame birds are
usually abraded and feathers are worn down. They may also have sternal bursitis.

5. Vent area is a good place to look for mites and for urates or feces matting feathers.

6. Crop contents. Distended hard crops (feed impaction) may indicate suffocation.
Empty crops indicates anorexia, one of the earliest indicators of illness in a bird.
Fluidfilled crops are seen when birds have a fever.

7. Bone integrity (humerus, femur, pelvis & keel bones).

8. Both lungs (color & consistency). For optimum microscopic examination, lungs need
to be fixed in situ (see avian proliferative pulmonary disease) and trimmed in a dorsal
plane adjacent to the main bronchus.

9. Heart size needs to be determined. If critical information is needed, weights of the

free right ventricle and left ventricle including septum can be determined. Examine
valves for endocardiosis.

10. Liver color, size, texture. Gall bladders that are distended (project beyond the
margin of the liver) and filled with dark bile indicate anorexia.

11. Examine reproductive tracts to determine the reproductive status of the birds. Check
females for number and atresia of hierarchal follicles. In a disease, atresia of follicles
begins with the largest one and continues until all follicles are atretic. Atresia of the first
follicle occurs within 24 - 36 hours of the onset of an acute disease. Yolk leaking from
follicles undergoing atresia causes diffuse mild (yolk) peritonitis. Distention of the ductus
deferens with semen, best seen as the ductus enters the urodeum of the cloaca,
coupled with testis size are good indicators that a male is in production. However,
semen stored in the ductus may persist for several days to weeks after production of
spermatozoa in the seminiferous tubules of the testes has ceased.

12. Urate deposition in joints and tissues indicates kidney disease. Also check ureters
for distention and blockage with calculi. Prominent kidneys that are otherwise normal in
appearance generally do not indicate a disease (Powell, 2004)

Early-lay Mortality

The house is prepared; feed, water, lighting, and ventilation are set; everything appears
to be in order. Roosters and pullets look good - the flock should do well. By week 25,
egg production increases and feed allocated to the birds is increased accordingly. As
egg production reaches 5%, they are switched to a high calcium breeder diet. During
week 26, hen mortality exceeds 0.4%; not alarming but it has increased daily during the
week. By the end of week 27, hen mortality has doubled, which peaks at 1.6% the
following week. Roosters are unaffected. By week 32, hen mortality declines to
expected levels as rapidly as it increased.

Although the poultry industry has learned ways to manage today's high-yield broiler
breeder strains, mortality during the early lay period between onset and peak of egg
production is still common and typically higher than later in the egg-laying cycle. Early
lay mortality results in substantial economic losses because of the lost investment in the
hen and unrealized production of hatching eggs and chicks. If it is high and
unanticipated, it can disrupt the production stream within a company. US industry
estimates the costs due to breeder mortality are $0.10 to $0.20 USD per pullet placed.
Losses from unrealized productivity amount to as much as $0.50 to $2.50 USD per hen
capitalized. For a 1 million broiler-processed per week operation, breeder hen mortality
losses could reach $1,000,000 USD per year.

Between 1994 and 2004, over 700 problem flocks in the US and South America
between 25 and 32 weeks of age were examined. Similarly, hen mortality of several
breeder flocks in Europe were categorized. Mortality ranged from 1-16% during this
period and averaged 4.2%. Most (40-60%) mortality was categorized as "metabolic",
with few lesions observed. During the early to mid 90's, much of this mortality was
associated with hens that had small frames and were under fleshed. More recently
mortality has been associated with heavy, over-conditioned hens. In both cases the
underlying cause of mortality could be attributed to poor early development, poor flock
body weight uniformity, and an accelerated feed-forproduction schedule, which resulted
in rapid late development that has both metabolic and reproductive consequences for
the hens (Powell, 2004).

In a study of early lay mortality in North Carolina, the most likely cause of death was
determined by necropsy in six broiler breeder flocks represented by two flocks each of
Arbor Acre Plus, Cobb 500, and Cobb 700. Hens that died during a single day each
week between 25 and 32 weeks of age were identified with the location where they
were found in the house, date and time, and farm. A total of 128 birds were necropsied:
29 Arbor Acre Plus birds, 35 Cobb 500 birds, and 64 Cobb 700 birds. Most of the
mortality (66%) resulted from non-infectious diseases including vent persecution
(cannibalism)/mate aggression, musculoskeletal disorders, calcium tetany, renal
disease, and crop impaction/choke. The greatest single cause of mortality was vent
persecution, which was especially prevalent in one flock. No cause of death was
determined for 12% of the hens. Infectious diseases (salpingitis, peritonitis,
arthritis/synovitis) accounted for 22% of the mortality (Boswell et al., 2008). Mortality
tended to be flock specific.

Current Broiler Breeder Diseases

In this presentation, it is only possible to briefly review a few of the current diseases
affecting broiler breeders that are of significance to the broiler industry. Enterococcal
spondylitis, staphylococcosis, impaired mobility ("calcium tetany"), cloacitis, feather
picking, avian proliferative pulmonary disease, avian hepatitis E virus infection, and
sporadic lymphoid leukosis were selected; there are many others that are important, but
could not be covered.

Enterococcal Spondylitis (ES). Enterococcal spondylitis (ES, vertebral osteomyelitis

[VOA], "Spinal Abscess") emerged as a disease of young male broiler breeders
(females are infrequently affected) caused by Enterococcus cecorum in the US in late
2006 (Aziz and Barnes, 2007). Since the initial case in breeders, additional breeder
flocks have continued to be affected in most poultry producing areas of the US and
Canada (Stalker et al., 2010), although the occurrence has declined in the past few
years. In late 2007 and 2008, the disease emerged in broiler flocks in the US.
Inflammatory musculoskeletal disease due to E. cecorum had previously been identified
in broilers in Europe (Devriese et al., 2002, Wood et al. 2002; De Herdt et al., 2008).
Often the disease reoccurs in the same house on a farm, but this is not consistent.
Thorough cleaning and disinfection (C&D) have proven useful in preventing ES in
subsequent flocks, but this also has not been consistent. Sometimes ES reoccurs
despite excellent C&D while other times it does not reoccur even when no special
treatment of the house is done between flocks.

Enterococcal spondylitis is characterized clinically by lameness, paresis, or paralysis.

Affected birds have a "sitting dog" or "kinky-back" appearance, move backwards when
approached, and may fall over on their side, unable to right themselves. Typically they
will have an arched back with a prominent dorsal keel (kyphosis) and appear shorter
than expected. They are bright, alert, and continue to eat and drink until they can no
longer access food or water. Less affected birds show weakness or unsteady gait. Birds
with serious clinical disease do not recover and must be culled, which can result in
losses as high as 15-20% in affected flocks. Breeder males as young as 4 weeks may
be affected, but most birds are between 8 and 14 weeks of age. Chronic lesions have
occasionally been found in roosters >50 weeks of age. Fertility is often below expected
levels when breeders come from a flock that had ES on the pullet farm. Presumably,
affected males that developed lesions survived, but were less capable of breeding
because of the spinal lesions.
At necropsy, a lesion is found in the free thoracic vertebra (T 4), the only articulating
bone in a chicken's thoracolumbar spine. It is essential to remove the lungs and
sometimes the kidneys of lame birds to visualize the spine, otherwise the lesion will not
identified. A large round to oval swelling will be found that can involve the cranial,
caudal, or both articulations of the free thoracic vertebra. Bits of lung typically adhere to
the surface of the lesion. When opened, the lesion is a cavity surrounded by dense
fibrous tissue and proliferating cartilage resembling a callus forming in response to a
fracture. The cavity is filled with crumbly necrotic material and inflammatory exudate. As
the lesion expands, the spinal cord is compressed. Occasionally, hemorrhage can be
seen in the spinal cord. Sagittal cuts of decalcified sections (10% formic acid) of
affected spines provide excellent visualization of lesions. ES lesions need to be
differentiated from spondylolisthesis ("kinky back") lesions.

Enterococcus cecorum is the most frequently isolated organism from spondylitis lesions.
In a recent study, 60% of spinal lesions yielded E. cecorum, 32% yielded
Staphylococcus spp., while there was either no growth or other bacteria from the
remaining lesions (Bunton et al., 2008). E. cecorum is infrequently isolated from other
inflammatory lesions of the musculoskeletal system, even from birds that have spinal
lesions from which E. cecorum is isolated.

Little is known about E. cecorum except that it is a normal inhabitant of the chicken's
intestinal tract. The lack of understanding about the pathogenesis of ES impedes our
ability to deal with the disease. Only a few male breeders developed lesions following
experimental inoculation with E. cecorum via intravenous, intra-air sac, or oral routes. A
subsequent study looking at the possible interaction of E. cecorum and coccidia also
resulted in limited reproduction of ES. Immunosuppression did not increase the rate of
lesion development (Stalker et al., 2010; Martin et al. 2011). It is likely E. cecorum gets
into the circulation following intestinal mucosal injury. Infection with attaching-effacing
Escherichia coli (AEEC) could be a predisposing factor as these are commonly found in
the ceca of birds with ES. However, the occurrence of AEEC in flocks without ES has
yet to be determined.

Staphylococcosis. Staphylococcosis is a well-known disease that still occurs frequently

and causes significant mortality in broiler breeder flocks. Males are most commonly
affected, females can develop the disease, but it is much less common. In males
staphylococcosis can account for as much as one-third of total mortality. Affected birds
are lame, typically underweight, and may be dehydrated. They have abraded wing tips,
sternal bursitis, arthritis, periarthritis, synovitis, tenosynovitis, or osteomyelitis. The
organism can also cause pneumonia, septicemia, hepatitis, vegetative valvular
endocarditis, orchitis, and skin and beak infections. Most outbreaks occur just prior to
sexual maturity, which is also a time when the birds receive multiple vaccinations. This
temporal relationship has led to the belief that vaccine inoculation introduces the
organism into the bird. However, we have found acute cases in birds throughout their
production cycle and that specific PFGE types cause the disease rather than a variety
of types as you would expect if Staphylococcus was an accidental contaminant.
Breeders with certain major histocompatibility complex types are more susceptible to
infectious skeletal disease cause by Staphylococcus (Joiner et al., 2005). Affected
males need to be culled. There is no prevention or treatment although careful handling
of the birds during weighing, vaccination, and moving may be helpful and good hygiene
during vaccination is still recommended.

Impaired mobility ("calcium tetany"). There can be many causes of impaired mobility in
breeder hens that require thorough evaluation to identify which of them may be
involved. Affected hens are frequently severely traumatized on their backs and heads
because of over-breeding by the males. The males are blamed and the problem is
identified as "rooster kill" or "mate aggression," but usually the real problem is impaired
mobility of the hens. Affected hens cannot escape the scratch area and their immobility
makes them appear receptive to males for breeding.

One cause of mobility impairment in hens is calcium tetany, an acute calcium imbalance
brought on by insufficient analyzer (i-STAT®) is a convenient way to measure ionized
calcium levels in the blood (Martin et al., 2010; 2011). Typically, early producing flocks
prior to peak lay (25-30 wks) are most affected. Hens show lethargy, tremors, panting,
cyanosis, paralysis, and death. Mortality may be up to 2%/wk for 1-2 weeks. At
necropsy, there are no internal gross lesions. Often there is an egg in the shell gland or
an indication that an egg has just been laid, visceral tissues are congested, lungs are
dark and may be edematous, and there may be pale streaks in the pectoral muscles.
Affected hens are in production and frequently super-ovulatory (≥ 8 active follicles). A
tentative diagnosis in a dead hen can be made on the basis of exclusion of any other
cause of mortality, hen in active production, and generalized congestion. Measuring
ionized blood calcium is not possible postmortem.

In clinical studies, calcium tetany was identified in one flock with mobility impaired hens,
but affected birds in other flocks had normal ionized calcium levels indicating there are
other causes of mobility impairment besides calcium tetany.

Cloacitis. Cloacitis associated with ulceration and hemorrhage has been observed in
broiler breeder flocks with excessive hen mortality. Hemorrhage from the cloaca initially
presents as bloodstained eggs. Bloody vents subsequently lead to vent pecking
mortality. Lesions can appear throughout the cloaca but are most highly concentrated
near the opening to the vagina. Affected birds appear otherwise healthy and
reproductively active. In affected flocks, up to 30% of healthy looking hens have been
observed with cloacal lesions. The disease tends to repeat on the same farm and
house. Often it develops within a few weeks of adding new males to a flock (Martin et
al., 2010).

Lesions vary in severity. Histologically, cloacitis is characterized by hemorrhages,

edema, acute heterophilic inflammation, increased lymphoid tissue, and epithelial
hyperplasia at the cloacalvaginal junction. Ulceration is seen in more advanced lesions.
Vaginitis may also occur, but it is not a consistent finding (Fletcher et al., 2010).
The cause remains unknown. Attempts to isolate Neisseria, Salmonella, and
Mycoplasma and demonstrate herpesvirus have been negative. A genusspecific
Mycoplasma PCR showed some positive results, but no viable mycoplasmas or
ureaplasmas could be isolated. Epidemiologically, cloacitis has a pattern suggestive of
a sexually transmitted disease, but the possibility that it is simply the result of trauma
from egg laying cannot be excluded. It is likely that vent pecking is preceded by cloacal
inflammation.

Feather pecking. Feather licking and feather eating have been reported in most broiler
breeder strains and can be observed in pullets and cockerels as early as 10 weeks of
age. These behaviors are considered normal, but they can progress to abnormal vices
such as vent pecking and cannibalism. Though there is more understanding of these
behaviors in layers, speculations as to the cause in broiler breeders include genetics
(Cutbertson, 1980; Rodenburg, et al., 2008; Wysocki et al., 2010); immune stimulation
(Parmentier, et al., 2009); light intensity and environment (Johnsen, et al., 1988); and
feed texture and density (van Krimpen, et al., 1988). Other lesions can be observed and
may be associated with feather pecking such as trauma to the cloaca predisposing to
cloacitis, as well as other maladies associated with heavy feed restriction (Powell, K.C.
2000).

Various treatments have been reported including acidification of the water, sodium
bicarbonate (Venne, et al., 2010), zinc/methionine supplements, vitamin/mineral
supplements, high fiber & lower energy diet formulations (van Krimpen et al., 2010),
spectacles/blinders, beak conditioning, and heavier male body weight targets during
rearing.

Avian proliferative pulmonary disease. A common finding when investigating metabolic

disorders or low egg production is finding lung lesions consisting of smooth muscle
hypertrophy and hypertrophy and hyperplasia of epithelial cells lining the parabronchi,
atria, and infundibula. Exudative pneumonia may or may not be present.

Critical evaluation of lung tissue is best done by leaving the lungs in the chest of the bird
and fixing the lungs, ribs, and spine together (in situ fixation). After 24 - 48 hours,
depending on the size of the tissues, the lungs can be removed from the chest cavity. In
situ fixation of the lungs permits morphometric analysis (Fletcher et al., 2008). Trimming
lungs in a dorsal plane (parallel to the spine) adjacent to the main bronchus is preferred
for demonstrating lesions. The caudal part of the lung where the main bronchus opens
into the caudal thoracic and abdominal air sacs is the most likely area for lesions to be
located.

Avian hepatitis E virus infection. Infections with hepatitis E virus (HepEV) are an
emerging problem in broiler breeders (Morrow et al., 2008). Affected flocks are
characterized by decreased production and increased mortality that begins between 40
and 45 weeks of age and continues until the end of the production cycle. Hatchability is
not affected. Hens have enlarged, irregularly patterned livers, and splenomegaly.
Sometimes bloody fluid or clotted blood is found in the body cavity. Histologically, there
is degeneration and inflammation occurring simultaneously in the liver that is
accompanied by marked myelopoiesis. Myelopoiesis can be so intense that HepEV
infection has been confused with myeloid leukosis caused by ALV-J virus. Hepatic
amyloidosis is common in some flocks, but not seen in others. Splenic hyperplasia with
numerous lymphoid nodules accounts for enlargement of the spleen. Histopathology is
characteristic but demonstration of the virus by PCR in bile samples is useful in
confirming HepEV infection. At present, no means of preventing HepEV infection is
known.

Sporadic lymphoid leukosis. Sporadic cases of lymphoid leukosis (LL) in a flock of

approximately 1100 broiler breeders were determined. All birds that died or were culled
from the flock were necropsied. LL was sporadic and only occurred in females. Flock
mortality due to sporadic LL was approximately 1%; however, it accounted for
approximately 6% of all mortality. Over half of the sporadic LL cases occurred between
30 and 40 weeks of age. Affected birds were in good body condition, but had small dark
combs, and were out of production. Ovaries of younger birds were tumorous and
undeveloped, whereas those in older birds showed tumors and were regressed. Lesions
were frequent in liver, spleen, kidney and bursa of Fabricius, but no tissue had tumors in
all affected birds. A few birds had tumors in bone resembling myeloid leukosis. Tumors
also occurred infrequently in proventriculus, thymus, and lungs. Microscopically,
sporadic LL lesions consisted of expanding nodules of large lymphocytes. No lesions
occurred in the central or peripheral nervous systems. The cause is unknown. Attempts
to identify a specific leukosis virus (A,B, D, J), reticuloendotheliosis virus, or Marek's
disease virus were unsuccessful. An interaction between serotype 2 Marek's disease
virus, for which the flock had been vaccinated, and an endogenous retrovirus was
suspected.