Broiler Breeder Diseases

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 (T₄), 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.

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 Breeder & Hatchery Management Conference, Statesville, NC, USA, October 29-30.

Chen, S.E., McMurty, J.P. & Walzem, R.L. (2006). Overfeeding-induced ovarian dysfunction in broiler breeder hens is associated with lipotoxicity. Poultry Science, 85,70-81.

Cutbertson, G. J. (1980). Genetic variation in feather-pecking behaviour. British Poultry Science, 21, 447–450.

De Herdt, P., Defoort P., Steelant, J. van, Swam, H., Tanghe, L., Goethem, S. van, et al. (2008) Enterococcus cecorum osteomyelitis and arthritis in broiler chickens. Vlaams Diergeneeskundig Tijdschrift, 78, 44- 48.

Devriese, L. A., Cauwerts, K., Hermans, K. & Wood, A.M. (2002). Enterococcus cecorum septicemia as a cause of bone and joint lesions resulting in lameness in broiler chickens. Vlaams Diergeneeskundig Tijdschrift, 71, 219-222.

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Fletcher, O.J., Martin, M.P., Barnes, H.J Ley, D.H., Marusak, R.A.& Robbins, K.M. (2010).

Bloody vents associated with cloacitis in broiler breeder flocks. II: Histopathology and other diagnostic tests. Proceedings of the American Association of Avian Pathologists Meeting, Atlanta, GA August 1-4.

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Joiner, K.S., Hoerr, F.J., Santen, E. Van & Ewald, S. J. (2005). The avian major histocompatibility complex influences bacterial skeletal disease in broiler breeder chickens. Veterinary Pathology, 42, 275-281.

Krimpen, M.M. van, Kwakkel, R.P., Reuvekamp, B.F.J., Peet-Schwering, C.M.C van der, Hartog, L.A. den, et al. (2005). Impact of feeding management on feather pecking in laying hens. World's Poultry Science Journal, 61, 663-685.

Krimpen, M.M. van. (2010). Dietary manipulation as a tool to prevent feather pecking in laying hens. Proceedings of the 2nd International Symposium - Highlights in Nutrition and Welfare in Poultry Production. Wageningen, The Netherlands.

Martin, L.T., Martin, M.P. & Barnes, H.J. (2011). Experimental reproduction of enterococcal spondylitis (ES) in male broiler breeder chickens. Avian Diseases, 55, 273-278.

Martin, M.P., Fletcher, O.J., Ley, D.H., Marusak, R.A., Robbins, K.M. & Barnes, H.J. (2010). Bloody vents associated with cloacitis in broiler breeder flocks. I: Field investigations, clinical description and epidemiology. Proceedings of the American Association of Avian Pathologists Meeting, Atlanta, GA August 1-4.

Martin, M.P., Wineland, M., Fletcher, O.J. & Barnes, H.J. (2011). Selected blood chemistry values in mobility impaired broiler breeder hens with suspected calcium tetany using the i-STAT® handheld clinical analyzer. Avian Diseases, 55, (In press).

Martin, M.P., Wineland, M., & Barnes H.J. (2010). Selected blood chemistry and gas reference ranges for broiler breeders using the i-STAT handheld clinical analyzer. Avian Diseases, 54, 1016-1020.

Morrow, C.J., Samu, G., Matrai, E., Klausz, A., Wood, A.M., Richter, S. et al. (2008). Avian hepatitis E virus infection and possible associated clinical disease in broiler breeder flocks in Hungary. Avian Pathology, 37, 527-535.

Parmentier, H. K., Rodenburg T. B., Reilingh, G, de V., Beerda, B. & Kemp, B. (2009). Does enhancement of specific immune responses predispose laying hens for feather pecking? Poultry Science, 88, 536-542.

Powell, K.C. (2000). Fertility and hatchability factors with broiler breeder males. Vineland Update 67, Vineland Laboratories, Vineland, NJ.

Powell, K.C. (2004). Early lay mortality in broiler breeders – causes, costs and solutions. Proceedings of the North Carolina Broiler Breeder & Hatchery Management Conference, Statesville, NC, USA.

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Roza, K., Martin, M. & Barnes, H. John. (2006). Litter impaction of the lower intestinal tract in male broiler breeders. Avian Diseases, 50, 460-462

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Venne, D., Itee, C.S. & Chorfi, Y. (2010). Clinical aspects of in-field use of a portable biochemistry instrument (I-STAT-1) in reducing feather picking and cannibalism in broiler breeders. Proceedings of the 59th Western Poultry Disease Conference, Sacramento, CA, USA.

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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