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The following technical article is related to the event:
XVII Congress of the World Veterinary Poultry Association

Broiler Breeder Diseases

Broiler Breeder Diseases - A Review
Published on: 07/23/2012
Author/s : Dr. Guillermo Zavala (Department of Population Health, College of
Veterinary Medicine, University of Georgia)and Dr. H. John Barnes (Poultry Health
Management Team, Department of Population Health and Pathobiology, College of
Veterinary Medicine, North Carolina State University)and Kenneth C. Powell
(Aviagen LLC)
(5031)
(6)

Summary
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-for production 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. cecorumis 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
ifStaphylococcus 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.
References
Aziz, T. & Barnes, H. J. (2007). Is spondylitis an emerging disease in broiler
breeders? World Poultry, 23, 44-45.
Aziz, T., Martin, M., Barnes, H.J. & Fletcher, O. (2010). Cloacitis: an emerging
problem in broiler breeder hens. World Poultry, 26 (8), 12-13.

Boswell, L.M., Wineland, M.J. & Barnes H.J. (2008). Causes of broiler breeder hen
mortality during the early lay period. Proceedings of the American Association of
Avian Pathologists Meeting, New Orleans, LA July 19-23.
Bunton, J.L., Martin, M.P. & Barnes H.J. (2008). Could spinal abscesses by why my
male breeder replacements can't walk? Proceedings of the North Carolina Broiler
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Chen, S.E., McMurty, J.P. & Walzem, R.L. (2006). Overfeeding-induced ovarian
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Cutbertson, G. J. (1980). Genetic variation in feather-pecking behaviour. British
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al. (2008) Enterococcus cecorum osteomyelitis and arthritis in broiler chickens.
Vlaams Diergeneeskundig Tijdschrift, 78, 44- 48.
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Fletcher, O.J., Martin, M.P., Barnes, H.J Ley, D.H., Marusak, R.A.& Robbins, K.M.
(2010).
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Table 1. Diseases of Broiler Breeders

Growing Period
I. Non-infectious diseases
a. Trauma
i. Ruptured tendons (non-infectious)
ii. Pathologic fractures

iii. Scratches/lacerations/bruises (feed restriction association)

iv. Suffocation (piling)
v. Handling trauma (vaccinations, weighing)
b. Vaccination reactions
i. Granulomatous myositis
c. Respiratory disease
i. Foreign body pneumonitis
ii. Avian proliferative respiratory disease
d. Ammonia toxicity
i. Respiratory disease
ii. Keratoconjunctivitis
e. Choke ("feed pack")
f. Nutritional cataracts
II. Infectious diseases
a. Infectious typhlitis
i. Cecal coccidiosis
ii. Histomoniasis
iii. Salmonellosis (paratyphoid)
b. Infectious spondylitis
i. Enterococcus cecorum (Epidemic spondylitis)
ii. Other bacteria (Sporadic spondylitis)
c. Arthritis/tenosynovitis

i. Staphylococcosis
ii. Mycoplasmosis (MS)
iii. Viral arthritis
d. Enteritis
i. Coccidiosis
ii. Viral enteritis
iii. Dysbacteriosis
iv. Intussusception
v. Lack of uniformity
e. Mycotic infections
i. Airsacculitis
ii. Pneumonia
iii. Other organs
f. Intestinal parasites
i. Roundworms
ii. Tapeworms

Laying Period
I. Non-infectious diseases
a. Traumatic
i. Equipment related
1. Entrapment (slats, feeders)

2. Head trauma (feeders)

ii. Aggression
iii. Breeding trauma
iv. Slat height leg injuries
v. Handling trauma (weighing, serology)
b. Starvation
c. Obesity
d. Cloacal impaction
e. Beak necrosis
f. Vent persecution (pecking)
i. Cloacitis, "avian hemorrhoids"
1. Vent peck-out
g. Vent gleet/polyuria/acid urine
h. Feather disorders
i. Impaired mobility
i. Hypocalcemia, calcium tetany
ii. Osteoporosis
iii. Femoral head degeneration/necrosis
iv. Myopathy
v. Ruptured tendons/fractures
vi. Plantar dermatitis, "Gnarly feet"
vii. Articular gout

j. Cardiomyopathy
i. Sudden death syndrome
ii. Over restriction/refeeding syndrome
iii. Cardiomegaly
k. Urolithiasis/renal microlithiasis/visceral gout
i. Persistent infectious bronchitis
ii. Hypercalcemia
iii. Hypervitaminosis D
iv. Dehydration
l. Rodent predation
m. Toxicities
i. Feed related
1. Sodium
2. Calcium
ii. Medications
1. Coccidiostats (ionophores)
2. Anthelmintics
iii. Other
II. Infectious diseases
a. Fowl cholera
b. Vegetative valvular endocarditis
i. Avibacterium endocarditidis

ii. Enterococcus
iii. Other
c. Other bacteria
i. Septicemia
d. Staphylococcosis
i. Arthritis
1. Amyloid arthritis
ii. Synovitis/tenosynovitis
iii. Septicemia/hepatitis
e. Mycoplasma synoviae infection
f. Respiratory diseases
i. Infectious bronchitis
ii. Avian paramyxovirus 1
iii. Infectious laryngotracheitis
iv. Infectious coryza
v. Mycoplasma gallisepticum infection
g. Hepatitis E virus infection
h. Fowl pox
i. Ophthalmitis
i. Bacterial
ii. Fungal
j. Intestinal parasites

i. Roundworms
1. Ascaridia
2. Heterakis
3. Capillaria
ii. Tapeworms
k. Avian intestinal spirochetosis
i. Fecal staining of eggs
l. Neoplasia
i. Marek's disease
ii. Avian leukosis
1. Lymphoid leukosis
2. Myeloid leukosis and related diseases (ALV-J infection)
3. Sarcoma
iii. Other neoplastic diseases
III. Reproductive diseases
a. Male
i. Orchitis/epididymitis
1. Escherichia coli
2. Salmonella
3. Staphylococcus
ii. Epididymal/testicular lesions
1. Cystic testes

a. Sodium toxicity
b. Other
2. Regression
3. Lymphocytic orchitis, epididymitis
4. Sperm granulomas
5. Epididymal lithiasis
b. Female
i. Ovary
1. Regression
a. Bursting atresia, yolk peritonitis (serositis)
2. Superovulation
3. Oophoritis
a. Viral
b. Bacterial
ii. Abdominal masses
1. Eggs (internal layer)
2. Mis-ovulation
3. Oviductal masses
iii. Salpingoperitonitis
1. Colibacillosis
2. Salmonellosis
3. Other bacteria

iv. Oviduct obstruction

1. Differentiate from salpingoperitonitis
v. Cloacal/vaginal prolapse
1. Obesity
vi. Cysts
1. Follicular
2. Infundibular
3. Paraoviductal
4. Right oviduct
vii. Egg drops
1. Infectious bronchitis
2. Avian paramyxovirus 1
3. Other paramyxovirus infections
4. Avian influenza
5. Avian encephalomyelitis
6. Egg-drop 76 (adenovirus)
7. Mycoplasmosis (MG, MS)
8. Nutrition/management
viii. Eggshell apex abnormality ("glass-top eggs")
1. Mycoplasma synoviae
2. Infectious bronchitis virus
ix. Neoplasia

1. Sporadic lymphoid leukosis

2. Adenomas/adenocarcinomas
3. Sex cord tumors
a. Precocious development

Foreign Animal Diseases

I. Newcastle disease/"Exotic Newcastle disease"
II. Avian influenza
This paper was presented at the XVII WVPA Congress. Cancun, Mexico 2011,
August 2011. Engormix.com thanks for this huge contribution.
Author/s

John Barnes
Professor, Poultry Health Management Diplomate, American College of Veterinary
Pathologists Diplomate, American College of Poultry Veterinarians

Dr. Guillermo Zavala

M.S., M.A.M, Ph.D. from the University of Georgia DVM and Speciality in Poultry
Production and Pathology from the Universidad Nacional Autnoma de Mxico
(UNAM). Dr. Zavala is involved in clinical service to the poultry industry, research in
avian diseases and teaching. His research involves avian tumor viruses,
immunosuppressive disease and broiler breeders.Dr. Zavala interacts actively with the
domestic poultry industry in Georgia, the United States and overseas.
(5031)
(6)

Anna Catharina Berge

Vollezele, Brabant, Belgium
Veterinary Doctor
Contact Professional

Berge Veterinary Consulting

Brabant, Belgium
Contact
Re: Forum : Broiler Breeder Diseases - A Review
07/24/2012 |
thank you for sharing this article about Broiler Breeder Diseases! I will use this one as
a first go to, when troubles strike...
(1)
(0)

Nitin Suryavanshi
Mumbai, Maharashtra, India
Consultant
Re: Forum : Broiler Breeder Diseases - A Review
07/24/2012 |
thanking you for such a informative article about Broiler Breeder Diseases. pls focus
more on EODES .[ERROTIC OVIPOSITION DEFECTIVE EGG SYNDROME],
THANKS
(0)
(0)

Anna Catharina Berge

Vollezele, Brabant, Belgium
Veterinary Doctor

Contact Professional

Berge Veterinary Consulting

Brabant, Belgium
Contact
Re: Forum : Broiler Breeder Diseases - A Review
07/24/2012 | Dear Nitin Suryavanshi,
I have never heard of EODES. Could you please explain what this is? Is it common in
India? Do you have any references or links about it?
Kind regards,
Curious Catharina
(0)
(0)

Nitin Suryavanshi
Mwanza, Mwanza, Tanzania
Re: Forum : Broiler Breeder Diseases - A Review
07/24/2012 |
dear anna
EODES is basically noticed in broiler breeders as a result of prolapse .high % of
double yolk eggs .,internal ovulation ,resulting in egg peritonitis and mortality. high
weight pullet t shows symptons of EODES,
thanks
(0)
(0)

Sudheer Rukadikar
Pune, Maharashtra, India
Veterinary Doctor
Contact Professional
Re: Forum : Broiler Breeder Diseases - A Review
07/29/2012 |

Thanks for good, informative article. However, all the disease or disease like
problems are described for broiler breeders in deep litter. In India, we have majority of
broiler breeders in cages. Do you have similar information for caged broiler breeders?
Cloacitis what is described in this article is seen in more sever form in few cases in
India. In some articles, it is described at "vent gleet". In caged breeders, there is no
question of aggression by male, but clacitis cases are seen in a few farms. Do you
have any such experience.
Thanks.
(0)
(0)

Analabs Limited
, , Kenia
Re: Forum : Broiler Breeder Diseases - A Review
08/07/2012 |
Is there any significant with +++epithelial cell in broilers
(0)
(0)
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