CAUSES OF DISEASE IN TWO COMMERCIAL FLOCKS OF LAYING HENS T. M. GRIMES*,B.V.Sc. Qireensland Department of Primary Industries, Arrimal Research Institute, Yeerongpilly, Queensland, 41 05 Introduction
One of the difficulties encountered when investigating production and disease problems in laying flocks is the evaluation of “background” disease which causes continuous low-level morbidity and mortality. Some indication of the causes of “background” disease can be obtained from autopsy examination of commercial hens at diagnostic laboratories, but the value of the results for this purpose is limited (Jordan 1956). The birds examined in such cases are usually a biased sample, as a particular disease is often occurring in the flocks at the time of examination, and the samples are collected accordingly. Autopsy examination of dead and cull hens from experimental flocks is also a source of disease information. However, the various experiments conducted probably influence the findings. Another means of obtaining data on disease is the compilation of slaughter-house condemnation reports, but this information has an age bias. In order to obtain more detailed information on the occurrence of “background” disease in commercial laying hens in Queensland, a morbidity and mortality study of 2 flocks was performed. Materials and Mdhods Birds The birds examined originated from two flocks, A and B. Both flocks were located on the same farm but in separate sheds (Table 1). Flock A contained hens of one strain and flock B contained hens of a different strain. The birds were reared as pullets on the growing farms of 2 breeding firms represented, prior to housing on the laying farm. The principal reason for selecting these flocks for study was that they were considered representative of current commercial operations producing eggs in Queensland. The examination which extended over a period of 8 months from May to December, 1973, was begun when flock A was 24 weeks of age and flock B was 21 weeks. Birds were removed from the flocks by the farm’s management if they appeared sick or died. Culling solely for poor production was not done. No acute disease outbreaks or production problems occurred in the flocks during the period of investigation. Laboratory Examination Cull and dead hens were collected from the farm 3 times weekly and autopsied. An attempt was made to f
Present address: ,Department. of Avian Medicine, College ,of Veterinary Medicme, Untverstty of Georgia, Athens, Georgia, United States of America 30602
Austrafian Veterinury Journal, Vol. 51. July, 1975
determine the reason for culling or death of each bird. This was referred to as the primary cause of disease. Many birds were found to have more than one cause of disease. Criteria for diagnoses were based on those given by Hofstad et al (1972) and Campbell (1969). Histopathological and microbiological examinations were performed when needed to assist in establishing a diagnosis. Swabs of lesions were cultured on blood agar plates incubated aerobically at 37°C. Tracheal mucus and caecal tonsil samples from birds with respiratory disease and kidney samples from birds with nephritis or visceral gout were inoculated into embryonated eggs and chicken kidney cell cultures, and examined for common avian respiratory viruses. Tracheal mucus was also inoculated on chocolate blood agar plates incubated in 5% COnat 37°C to detect Haemophilus gallinarum, and was cultured for Mycoplasma sp (Rosenfeld 1971). Microbiological isolations were attempted on 38 birds from flock A and 27 from flock B. Tissue sections obtained from 520 birds from flock A and 194 from flock B were subjected to histopathological examination. The majority of histopathological examinations were to classify tumours. One hundred and forty-nine hens from flock A were culled or died between 20 and 24 weeks of age, but were not examined as these losses occurred prior to the commencement of the investigation.
Results
The primary causes of disease and their frequency of occurrence are summarised in Table 2. Various causes of disease were more prevalent
I ~ Y I EI
PR(VALV~C )*
ksm
a
Roy
OuIn *Lm 1
oc
Figure 1. Prevslance of causes of disease in hens from Flock A.
337
TABLE 1
History and Management of the 2 Laying Flocks Examined
*
Observation
Flock A*
Flock B
No. of birds when housed in 3-4 bird cages on the laying farm Age at housinfi Feed program as pullets Feed program on the laying farm
17,000 20 weeks
full-fed full-fed
17,000 21 weeks
Feeding system Watei ing system Ration
automatic auger hart cups Commercial Firm A
kicch A
HR\
housed in
d
sepdraie shed to Flock B
at difkrent ages (Figures 1. 2 and 3 ) . More than one kind of neoplasm occurred in many birds (Table 3 ) . Observations and details of the major causes of loss are givcn below. Marek's Disease ( M L ) ) Forty-nine per cent of birds diagnosed at autopsy as having MD were culled due to unthriftyness, lameness, paralysis or respiratory sign+. The remainder were submitted dead. Turnours were found in most tissues, including the viscera, nerves, skin, muscles, eyes, thymus gland, bursa of Fabricius and brain. Twentyseven per cent of birds diagnosed as having M D had tumours predominantly in the ovary and mcsentery and had ascites. The coeliac nerve plexus appeared to be enlarged in many of these birds, but because of extensive thickening of the mesentery it was difficult to determine if the autooomic nerves were involved. Lesions in the nerves or brain were found in 32% of birds diagnosed as having MD. Colibacillosis was present in S % of the birds that had MD. En-
largement of the bursa due to a diffuse thickening of the wall, which often enclosed a necrotic adherent cast, or a small (1.0 - 1.5 cm) solid tumour was found in 5 % of birds with MD. Intestinal obstruction due to lesions of M D in the caecal tonsil was found in 3% of affected birds. Only 3% of birds with MD were in production when submitted. Lymphoid Leucosis Most birds diagnosed as having lymphoid leucosis were emaciated, had diarrhoea and had tumours in the liver, spleen, kidneys, bursa of Fabricius and ovary. Tumours were also found in the mesentery and intestine of some birds. Bursal involvement ranged from a small (0.5 cm) discrete nodule on the inner surface to multiple confluent tumours causing a solid bursa 1-7 cm in diameter. Bursal tumours were not found in 6% of birds with lesions of lymphoid leucosis. Obstruction of the large intestine or oviduct was caused by bursa1 tumours in some birds. Haeni angiomas The majority of birds with haemangiomas had haemorrhaged from ruptured haemangiomas.
_ _.- -. -_ .-
j r
quantitative feed restriction quantitative feed restriction until 10% egg production manual nipples Commercial Firm B
,I '
i
_ _ _ LYMPHOID LEUCQSES - - - HAEMANGIQML -SARCOMAS - - M I E L O I D LELCOfZS
I
AGE FIGURE 3. I CURL
2
~REI.LC*CE OF C I U S L I 01 0,)EIIIE i" WLLS T*OY r w c x B
Figure 3. F,pure 2
33X
Prevalence of causes of disease in hens from Flock 8.
IN
WEEKS
OF THE MOST FREQUENTLY OCCURRINO LEUCOSES AND SARCOMAS IN WENS FROM FLOCK A PREVALENCE
Prevalence of the most frequantly occurring IeUCOSeS and sarcomas in hens from Flock A.
Australian Veterinary Joimtal, Vol. 51. July, 1975
TABLE 2 Occurrence of Primary Causes of Disease Cause Marek‘s disease Leucoses and Sarcomas: Lymphoid leucosis Haernangioma Sarcomas Myeloid leucosis Hepatoma and hepatic carcinoma Nephroblastoma Total Other tumours : Adenoma and adenocarcinoma of the reproductive tract Granulosa cell tumour of the ovary Adenoma of the eye Astrocytoma of the brain Medulloblastoma of the brain Adenocarcinoma of the kidney Leiomyosarcoma Rhabdom yosarcoma Dysgerminoma of the ovary Carcinosarcoma Unidentified tumours
Flock A (24-57 Weeks)
Flock B (21-49 Weeks)
361
349
371 228 36 23 9 2
11 9 5 1 0 0
669
26
13
2
2 0 0
2 1
1 0 0
Total
28
8
Prolapse and cannibalism of the vent Cage layer fatigue Fatty liver syndrome Inflammation of the reproductive tract and viscera including “egg peritonitis” and colibacillosis Trauma and fracture of limbs Nephritis and visceral gout Inflammation of the skin Arthritis and synovitis Middle ear infection Respiratory disease Cystic reproductive tract Ruptured organs Cannibalism Starvation and dehydration Other Decomposed
347 127 81
131 29 34
90 37 13 5 4 0 5 13 5 0 16 194
42 19 10 5 9 1 0 2 9 4 52 7 29
Total
2,000
766
These birds were in good condition, were in production and had clinical signs of anaemia. Other birds which were in poor body condition had multiple haematomas and scar tissue where visceral haemangiomas had ruptured, but the resulting haemorrhage had been contained by the surrounding tissue. Haemangiomas were found in a wide range of tissues (Table 4). Matted blood on the feathers often indicated a haemangioma of the skin. Birds with haemangiomas in the upper respiratory tract or upper alimentary tract had blood clots in the nostrils, mouth, pharynx and larynx, oesophagus or crop. Haemopericardium occurred due to ruptured haemangiomas of the myocardium. Histological lesions Ai~stra/ianVeterinary Jorrrnal, Vol. 51. July, 1975
5
included both cavernous and capillary haemangiomas in the same tumour or in different tumours in the same bird. Undifferentiated endothelial and sarcomatous tissue was also present in many tumours. Sarcomas Sarcomas were found in .he skin (25), lungs ( 18), liver ( 1 3 ) , kidney ( 1l), skeletal muscle ( l o ) , ovary ( 7 ) , heart ( 6 ) , pleura ( 3 ) , mesentery ( 3 ) , peritoneum (2), intestine ( 2 ) and bursa of Fabricius ( 1) . They included fibrosarcomas, histiocytic sarcomas, myxosarcomas, and histiocytic and fibroblastic (mixed-cell) sarcomas. Ulceration, accompanied by haemorrhage and 339
TABLE 3 Occurrence oj Tumours in Birds With More Than I Turnour Type Primary Diagnosis
No. of Birds
Other Tumours Lymphoid Leucosis
Haemangiomas
sarcomas
NePhroblastoma
Miscellaneous
4
2
1
Lymphoid leucosis
24
21
5
2
adenocarcinoma of the pancreas
Haernangiomas
12
5
5
1
Sitr.comas
12
4
10
granulosa cell tumour (1) and teratoma ( 1 ) of the ovary osteochondrosarcoma
2
1
3
Mareh's disease
fi broleiomyoma of the oviduct (1)
(10)
Myeloid leucosis Nephroblastoma Hcpatic carcinoma
1 I
1
1
bacterial invasion, occurred in some skin sarconins. Most birds given a primary diagnosis of sarcomas had non-functional ovaries. doid LeucoAisTissues affected were kidneys (21), liver (17), ovary (15). skin (71, spleen ( 6 ) , muscle (4), mesentery (4), pleura (4),peritoneum ( 2 ) , intestine ( 2 ) and lung ( 1). Solid caseous yolks were found in birds with ovarian involvement, although similar lesions were also present in birds affected with ovarian abnormalities due to causes other than myeloid leucosis.
Mi
Prolapse m d Cunnibulisnz of the Vent Most birds with prolapse and cannibalism were i n good condition or were obese, were in pro-
duction and appeared to die from acute blood loss. Others had necrosis of the cloaca, and some of these had acute salpingitis. One per cent of birds with a primary diagnosis of prolapse and cannibalism had chronic salpingitis. Cage Layer Fatigue Birds diagnosed as having cage layer fatigue were dehydrated, and had greenish-white diarrhoea, brittle or broken bones, enlarged deformed costochondral junctions, haemorrhage into the tissues surrounding joints, and degenerating yolks in the ovary. Fntty Liver Syndrome Most birds that died of fatty liver syndrome had haemorrhaged severely from the liver into
TABLE 4 Tissue Distribution and Occurrence of Haemangiomas* Upper Alimentary and Respiratory Tract
Viscera ~~
I iver Kidney 0v'ir.l.
Me\enter) I unpc 5pleen Heart
740
Skin
122 54 25 18 It 11
8 8 1
(>vlducl
Infertine Totdl * Total number
Skeletal Muscles
~
~~~
4 Oesophagus 1 Pharynx and Larynx 8 Crop
258 of liens
H ifh
13
Muscles
32 32
Feet Body Legs Neck Wings
61 42
Vent
13 7
Face Comb and Wattles
37 23 17
5 205
haemangiomas - 211
Australian Veterinary Journal, Vol. 51. July, 1975
the abdominal cavity. There was evidence of previous ruptures of the liver in 7% of birds diagnosed as having fatty liver syndrome. Ninetysix per cent of birds with fatty liver syndrome were obese and were in production at the time of death. Histological lesions in the liver included widespread fatty change, multiple focal necrosis and haemorrhage. The macroscopic enlargement of the liver appeared to be due to a combination of intracellular fat deposition and haemorrhage. Starvation and Dehydration An arithmetical error made in the quantitative feed restriction program employed in flock B resulted in losses due to starvation and dehydration. The birds were emaciated, dehydrated, had hydropericardium, ascites, distended gall bladders and atrophied viscera, and were reluctant to walk or were recumbent. Miscellaneous Staphylococcus aureus was the organism most commonly isolated from birds with inflammation of the skin and from birds with arthritis and synovitis. Staph. aureus and Escherichia coli were isolated from birds with inflammation of the reproductive tract and viscera and from birds with nephritis. H. gallinarum was isolated from the trachea of 2 birds with respiratory disease. No viruses were detected in the trachea or caecal tonsil of birds with respiratory disease or from the kidneys of birds with nephritis and visceral gout. Discdon
Although strict comparisons between the prevalence of causes of morbidity and mortality in the 2 egg producing flocks are not valid in the absence of controls and replicates, some indication of trends can be gauged. The average weekly total of diseased birds in flock A (60.69) was greater than that in flock B (27.37). This resulted from a much higher incidence of leucoses and sarcomas and marginally greater losses due to prolapse and cannibalism, fatty liver syndrome and cage layer fatigue (Figures 1 and 2 ) . The prevalence of Marek‘s disease at different ages was similar in both flocks, and decreased markedly at 2 5 - 2 6 weeks of age. However, the prevalence of fatty liver syndrome at various ages differed between the 2 flocks. This could have been due to the different feeding programs used and may be related to reproductive maturity, as losses due to fatty liver syndrome increased in both flocks 10 - 12 weeks after 50% egg production was attained. Prolapse and cannibalism may also be correlated with reproductive maturity as it did not occur until birds were in lay. Austrulian Vereririnry Journal, Vol. 51. July, 1975
A similarity between the prevalence of lymphoid leucosis and haemangiomas at different ages was observed (Figure 3). Experimentally, the pathological response to leucoses and sarcoma viruses depends on the strain and dose of virus, the route of inoculation, the strain of bird and the age and sex of the bird (Purchase and Burmester 1972). Haemangiomas have been reproduced with a number of strains of leucosis virus (Purchase and Burrnester 1972), and recently Henderson et al (1974) incriminated an avian leucosis virus in field outbreaks of solid tumours, including haemangiomas. The histopathological variability of haemangiomas may be the reason for the existence of a number of synonyms for this tumour (Purchase and Burmester 1972). The high incidence of leucoses and sarcomas found in flock A was unexpected, as the high mortality of this strain of bird as pullets and in the first 6 months of lay was generally attributed to Marek‘s disease. Field and laboratory autopsy examinations of birds of this strain also suggested that fatty liver syndrome would be a more significant cause of loss in flock A. It is possible that the diagnosis of fatty liver syndrome had been confused on occasions, in previous examinations, with other causes of abdominal haemorrhage, particularly haemangiomas. The diagnosis of tumours of lymphoreticular cells was based on currently existing criteria (Purchase and Burmester 1972). Of these criteria, the finding of nerve lesions, the cellular morphology of tumours and the histopathological pattern of bursal tumours used separately or in combination were considered particularly useful in differentiating lymphoid leucosis and Marek’s disease. Bursal tumours occurred commonly in lymphoid leucosis, but infrequently in Marek’s disease. The bursal follicles were tumorous in lymphoid leucosis but cystic or necrotic in Marek‘s disease. Thickening of the bursal wall in those birds having bursal lesions of Marek’s disease was due to infiltration of lymphoreticular cells in the interfollicular septa. The adherent necrotic casts found in the lumen of some bursae appeared to result from cystic degeneration of bursal follicles causing accumulation of necrotic cellular debris. Bursal lesions, including cystic degeneration and necrosis of follicles, have been recorded in birds with experimentally reproduced Marek’s disease (Purchase and Biggs 1967; Purchase et a1 1968; Jakowski et a1 1969; Jakowski et a1 1970; Evans el ui 1971; Fletcher et al 1972). The tumours of lymphoid leucosis consisted mainly of large lymphoblasts which gave 341
the tumours a uniform, lightly basophilic appearance histologically. Marek‘s disease tumours were le5s uniform and more densely basophilic due to the pleomorphic cell population of small and medium lymphocytes, lymphoblasts, and plasma cells. These differential features were not readily detected once post-mortem decomposition had occurred. Xerve lesions in birds with Marek‘s disease were not found as frequently as expected. Goodchild ( 1969), in an extensive summary of nerve lesions in 502 field cases of classical Marek’s disease, found macroscopic neural lesions in almost 100% of birds. Purchase and Biggs ( 1967) reported that macroscopic nerve lesions were seen in SO% of chickens infected with isolates of acute Marek’s disease virus, although the frequency of occurrence of macroscopic nerve lesions in birds infected with an isolate of classical Marek’s disease virus was higher. One of the reasons for the apparent discrepancy between these results and those reported here could be the difficulty in evaluating autonomic nerve lesions in birds with extensive visceral tumours. particularly in the mesentery. The possibility that an agent other than Marek’s disease virus causes pleomorphic cell-type lymphomas in the viscera of adult hens cannot be overlooked. Macroscopic identification of tumours was digcult. This was particularly true with lymphoreticular cell turnours, sarcomas, myeloid leucosis, adenocarcinoma of the reproductive tract, granulosa cell tumours of the ovary and dysgerminomas of the ovary. Although some general indication of the tumour type could be obtained from the niacroscopic appearance and tissue distribution. it was concluded from this investigation that histopathological examination is required for accurate diagnosis of tumours. This could become particularly important in diagnosing tumours in birds vaccinated against Marek’s disease. Obesity has been incriminated as a contributing cause in fatty liver syndrome (Hofstad et a1 1972). In the investigation reported here, birds affected with fatty liver syndrome and prolapse and cannibalism appeared to have excess body fat. It is possible that a high incidence of disease in a flock due to these causes indicates that the laying flock as a whole is obese and may have inefficient feed conversion with respect to egg production. It was suspected that the peak Occurrence of cage layer fatigue in flock A at 41 - 45 weeks of age resulted from the settling out of the calciumphosphorous supplement added to the vegetable 31’
protein based ration. The possibility that the automatic auger feeding system and the coarseness of the mash assisted this sedimentation was considered likely. Excessively fluid faeces was a problem in flock A. Among the causes of “watery droppings” are lymphoid leucosis, cage layer fatigue and inflammation of the reproductive tract and viscera. The prevalence of these was higher in flock A than in flock B. Acute abdominal haemorrhage resulted mainly from fatty liver syndrome and haemangiomas, although less frequent causes were lymphoid leucosis, Marek’s disease, sarcomas and hepatic carcinomas. Blood clots in the oviduct were found in some birds with haemangiomas of the oviduct, abdominal haemorrhage and prolapse and cannibalism. This resulted in bloodstained eggs. The most common cause of visceral gout was chronic nephrosis and nephritis, other causes being tumours of the kidney, and tumours of the bursa of Fabricius or posterior peritoneal wall causing obstruction of the ureters. An upright posture and a “duck-walking” gait were features of birds with large tumours of the viscera, especially due to lymphoid leucosis, marked ascites, particularly in Marek’s disease, “egg-peritonitis”, and cystic oviduct. Paralysis and ataxia were seen in birds affected with Marek‘s disease, cage layer fatigue, tumours of the kidneys, leg muscles, shanks or feet, trauma and fracture of limbs, arthritis and synovitis and general debility. Abnormalities of the head and neck posture, such as torticollis, kyphosis and tremour, occurred due to brain lesions of Marek’s disease, medulloblastoma and astrocytoma, and in middle ear infection. Summary
Laboratory examination of all birds that were culled or died during an eight-month period in two commercial laying flocks was performed to reveal the causes of disease and their prevalence. The average weekly total of diseased birds was greater in one flock (60.69) than the other (27.37). This resulted mainly from a high incidence in the former flock of leucoses and sarcomas, although losses due to fatty liver syndrome, prolapse and cannibalism and cage layer fatigue were also marginally greater in this flock than the second. Haemangiomas occurred more frequently in the flock with the higher disease level. A total of 273 hens of the 2,000 examined from this flock had single or multiple haemangiomas. Special features of the major causes of disease were outlined and discussed. Australian Veterinury Journal, Vol. 51. July, 1975
A conclusion made from this study was that histopathological examination is necessary for accurate diagnosis of avian tumours. Referencm Campbell, J. G. (1969) -“Tumours of the Fowl”. 1st ed, William Heinemann Medical Books Limited, London. Evans, D. L., Beasley, J. N. and Patterson, L. T. (1971) - A v i a n Dis. 15:. 680. ._._ Fletcher, O . J . , Eidson, C. S. and Kleven, S. H. (1972) -Avian Dis. 16: 153, Goodchild. W. M. (1969) - V e t . Rec. 84: 87. Henderson, B. E., Gardner, M. B., Charman, H. P., Johnson, E. Y., Rucio, T., Sarma, P., Alena, B. and Huebner, R. J. (1974) -Avian Dis. 18: 58.
Hofstad, M. S., Calnek, B. W., Helmboldt, C. F., Reid, W. M., Yoder, H. W. (1972) “Diseases of Poultry”. 6th ed, Iowa State University Press, Ames. Jakowski, R. M., Fredrickson, T. W., Chomiak, T. W. and Luginbuhl, R. E. (1970) -Avian Dis. 14: 374. Jakowski, R. M., Fredrickson, T. W., Luginbuhl, R. E. and Helmboldt, C. F. (1969) --Avian Dis. 13: 215. Jordan, F. T. (1956) -J. comp. Path. 66: 197. Purchase, H. G . and Biggs, P. M. (1967) -Res. vet. Sci. 8 : 440. Purchase, H. G. and Burmester, B. (1972) -In “Diseases of Poultry”. Ed. by M. S. Hofstad, 6th edn, Iowa State University Press, Ames. Purchase, H. G., Chubb, R. C. and Biggs, P. M. (1968) -J . natn. Cancer Inst. 40: 583. Rosenfeld, Lorraine E. (1971) Aust. vet. J . 47: 492. (Received for publication 10 July 1974)
-
-
BOOK REVIEW THE PRINCIPLES OF HORSESHOEING ‘Horseshoeing’, Anton Lungwitz is quoted as having written at the turn of the twentieth century, ‘is an industry which requires, in equal degree, knowledge and skill.’ Butler’s excellent text* will go far in assisting those interested in attaining at least the first of these requirements. The author suggests, in his first chapter, that the number of horses in the United States of America after a low of 3,000,000 in 1960 will reach 16,000,000. by. 1980. This increasing popularity of horses, which IS probably common to many developed countries, is just one indication of the need for an up-to-date manual o n this ancient art. The subject matter covers many aspects of the horse’s hoof and its maintenance, including an interesting introduction describing some of the superstitions and folk-lore surrounding farriers and their craft. Written by an obviously dedicated expert, the chapters include the anatomy of the hoof, horse handling and forge techniques; the latter subject being dealt with quite extensively. The notes on corrective shoeing are presented *The Principles of Horseshoeing. Dou Butler. Published by Doug Butler, 1611 East Shore Drive, fthaca, NY, USA, 1974 Pp. 428 $19.95.
Australicin Ve/erinary Journal, Vol. 5 1. July, 1975
logically and are well illustrated; they should be valuable for the veterinarian searching for the correct types of shoe to use in the treatment of various hoof and leg conditions. The author has managed fairly well to bridge the gap between horseman and veterinarian in this area of treatment, without arming the layman with too much potentially ‘dangerous’ pharmacological knowledge. A strong feature of the book is the methodical clearcut layout, with each subject clearly defined and presented in an easily followed form. The diagrams are excellent and are used to great advantage. Likewise, the photographs are of good quality and add to the readability of the text. The index is refreshingly comprehensive - nowadays indexes can be more frustrating than helpful! A helpful list of general references is given. This is a good functional book, and, although unfortunately fairly expensive, is well worth the consideration of those who require an extensive knowledge of the horse’s hoof, as well as those looking for a practical manual of horseshoeing. C. D. Mackenzie
343
One of the difficulties encountered when investigating production and disease problems in laying flocks is the evaluation of “background” disease which causes continuous low-level morbidity and mortality. Some indication of the causes of “background” disease can be obtained from autopsy examination of commercial hens at diagnostic laboratories, but the value of the results for this purpose is limited (Jordan 1956). The birds examined in such cases are usually a biased sample, as a particular disease is often occurring in the flocks at the time of examination, and the samples are collected accordingly. Autopsy examination of dead and cull hens from experimental flocks is also a source of disease information. However, the various experiments conducted probably influence the findings. Another means of obtaining data on disease is the compilation of slaughter-house condemnation reports, but this information has an age bias. In order to obtain more detailed information on the occurrence of “background” disease in commercial laying hens in Queensland, a morbidity and mortality study of 2 flocks was performed. Materials and Mdhods Birds The birds examined originated from two flocks, A and B. Both flocks were located on the same farm but in separate sheds (Table 1). Flock A contained hens of one strain and flock B contained hens of a different strain. The birds were reared as pullets on the growing farms of 2 breeding firms represented, prior to housing on the laying farm. The principal reason for selecting these flocks for study was that they were considered representative of current commercial operations producing eggs in Queensland. The examination which extended over a period of 8 months from May to December, 1973, was begun when flock A was 24 weeks of age and flock B was 21 weeks. Birds were removed from the flocks by the farm’s management if they appeared sick or died. Culling solely for poor production was not done. No acute disease outbreaks or production problems occurred in the flocks during the period of investigation. Laboratory Examination Cull and dead hens were collected from the farm 3 times weekly and autopsied. An attempt was made to f
Present address: ,Department. of Avian Medicine, College ,of Veterinary Medicme, Untverstty of Georgia, Athens, Georgia, United States of America 30602
Austrafian Veterinury Journal, Vol. 51. July, 1975
determine the reason for culling or death of each bird. This was referred to as the primary cause of disease. Many birds were found to have more than one cause of disease. Criteria for diagnoses were based on those given by Hofstad et al (1972) and Campbell (1969). Histopathological and microbiological examinations were performed when needed to assist in establishing a diagnosis. Swabs of lesions were cultured on blood agar plates incubated aerobically at 37°C. Tracheal mucus and caecal tonsil samples from birds with respiratory disease and kidney samples from birds with nephritis or visceral gout were inoculated into embryonated eggs and chicken kidney cell cultures, and examined for common avian respiratory viruses. Tracheal mucus was also inoculated on chocolate blood agar plates incubated in 5% COnat 37°C to detect Haemophilus gallinarum, and was cultured for Mycoplasma sp (Rosenfeld 1971). Microbiological isolations were attempted on 38 birds from flock A and 27 from flock B. Tissue sections obtained from 520 birds from flock A and 194 from flock B were subjected to histopathological examination. The majority of histopathological examinations were to classify tumours. One hundred and forty-nine hens from flock A were culled or died between 20 and 24 weeks of age, but were not examined as these losses occurred prior to the commencement of the investigation.
Results
The primary causes of disease and their frequency of occurrence are summarised in Table 2. Various causes of disease were more prevalent
I ~ Y I EI
PR(VALV~C )*
ksm
a
Roy
OuIn *Lm 1
oc
Figure 1. Prevslance of causes of disease in hens from Flock A.
337
TABLE 1
History and Management of the 2 Laying Flocks Examined
*
Observation
Flock A*
Flock B
No. of birds when housed in 3-4 bird cages on the laying farm Age at housinfi Feed program as pullets Feed program on the laying farm
17,000 20 weeks
full-fed full-fed
17,000 21 weeks
Feeding system Watei ing system Ration
automatic auger hart cups Commercial Firm A
kicch A
HR\
housed in
d
sepdraie shed to Flock B
at difkrent ages (Figures 1. 2 and 3 ) . More than one kind of neoplasm occurred in many birds (Table 3 ) . Observations and details of the major causes of loss are givcn below. Marek's Disease ( M L ) ) Forty-nine per cent of birds diagnosed at autopsy as having MD were culled due to unthriftyness, lameness, paralysis or respiratory sign+. The remainder were submitted dead. Turnours were found in most tissues, including the viscera, nerves, skin, muscles, eyes, thymus gland, bursa of Fabricius and brain. Twentyseven per cent of birds diagnosed as having M D had tumours predominantly in the ovary and mcsentery and had ascites. The coeliac nerve plexus appeared to be enlarged in many of these birds, but because of extensive thickening of the mesentery it was difficult to determine if the autooomic nerves were involved. Lesions in the nerves or brain were found in 32% of birds diagnosed as having MD. Colibacillosis was present in S % of the birds that had MD. En-
largement of the bursa due to a diffuse thickening of the wall, which often enclosed a necrotic adherent cast, or a small (1.0 - 1.5 cm) solid tumour was found in 5 % of birds with MD. Intestinal obstruction due to lesions of M D in the caecal tonsil was found in 3% of affected birds. Only 3% of birds with MD were in production when submitted. Lymphoid Leucosis Most birds diagnosed as having lymphoid leucosis were emaciated, had diarrhoea and had tumours in the liver, spleen, kidneys, bursa of Fabricius and ovary. Tumours were also found in the mesentery and intestine of some birds. Bursal involvement ranged from a small (0.5 cm) discrete nodule on the inner surface to multiple confluent tumours causing a solid bursa 1-7 cm in diameter. Bursal tumours were not found in 6% of birds with lesions of lymphoid leucosis. Obstruction of the large intestine or oviduct was caused by bursa1 tumours in some birds. Haeni angiomas The majority of birds with haemangiomas had haemorrhaged from ruptured haemangiomas.
_ _.- -. -_ .-
j r
quantitative feed restriction quantitative feed restriction until 10% egg production manual nipples Commercial Firm B
,I '
i
_ _ _ LYMPHOID LEUCQSES - - - HAEMANGIQML -SARCOMAS - - M I E L O I D LELCOfZS
I
AGE FIGURE 3. I CURL
2
~REI.LC*CE OF C I U S L I 01 0,)EIIIE i" WLLS T*OY r w c x B
Figure 3. F,pure 2
33X
Prevalence of causes of disease in hens from Flock 8.
IN
WEEKS
OF THE MOST FREQUENTLY OCCURRINO LEUCOSES AND SARCOMAS IN WENS FROM FLOCK A PREVALENCE
Prevalence of the most frequantly occurring IeUCOSeS and sarcomas in hens from Flock A.
Australian Veterinary Joimtal, Vol. 51. July, 1975
TABLE 2 Occurrence of Primary Causes of Disease Cause Marek‘s disease Leucoses and Sarcomas: Lymphoid leucosis Haernangioma Sarcomas Myeloid leucosis Hepatoma and hepatic carcinoma Nephroblastoma Total Other tumours : Adenoma and adenocarcinoma of the reproductive tract Granulosa cell tumour of the ovary Adenoma of the eye Astrocytoma of the brain Medulloblastoma of the brain Adenocarcinoma of the kidney Leiomyosarcoma Rhabdom yosarcoma Dysgerminoma of the ovary Carcinosarcoma Unidentified tumours
Flock A (24-57 Weeks)
Flock B (21-49 Weeks)
361
349
371 228 36 23 9 2
11 9 5 1 0 0
669
26
13
2
2 0 0
2 1
1 0 0
Total
28
8
Prolapse and cannibalism of the vent Cage layer fatigue Fatty liver syndrome Inflammation of the reproductive tract and viscera including “egg peritonitis” and colibacillosis Trauma and fracture of limbs Nephritis and visceral gout Inflammation of the skin Arthritis and synovitis Middle ear infection Respiratory disease Cystic reproductive tract Ruptured organs Cannibalism Starvation and dehydration Other Decomposed
347 127 81
131 29 34
90 37 13 5 4 0 5 13 5 0 16 194
42 19 10 5 9 1 0 2 9 4 52 7 29
Total
2,000
766
These birds were in good condition, were in production and had clinical signs of anaemia. Other birds which were in poor body condition had multiple haematomas and scar tissue where visceral haemangiomas had ruptured, but the resulting haemorrhage had been contained by the surrounding tissue. Haemangiomas were found in a wide range of tissues (Table 4). Matted blood on the feathers often indicated a haemangioma of the skin. Birds with haemangiomas in the upper respiratory tract or upper alimentary tract had blood clots in the nostrils, mouth, pharynx and larynx, oesophagus or crop. Haemopericardium occurred due to ruptured haemangiomas of the myocardium. Histological lesions Ai~stra/ianVeterinary Jorrrnal, Vol. 51. July, 1975
5
included both cavernous and capillary haemangiomas in the same tumour or in different tumours in the same bird. Undifferentiated endothelial and sarcomatous tissue was also present in many tumours. Sarcomas Sarcomas were found in .he skin (25), lungs ( 18), liver ( 1 3 ) , kidney ( 1l), skeletal muscle ( l o ) , ovary ( 7 ) , heart ( 6 ) , pleura ( 3 ) , mesentery ( 3 ) , peritoneum (2), intestine ( 2 ) and bursa of Fabricius ( 1) . They included fibrosarcomas, histiocytic sarcomas, myxosarcomas, and histiocytic and fibroblastic (mixed-cell) sarcomas. Ulceration, accompanied by haemorrhage and 339
TABLE 3 Occurrence oj Tumours in Birds With More Than I Turnour Type Primary Diagnosis
No. of Birds
Other Tumours Lymphoid Leucosis
Haemangiomas
sarcomas
NePhroblastoma
Miscellaneous
4
2
1
Lymphoid leucosis
24
21
5
2
adenocarcinoma of the pancreas
Haernangiomas
12
5
5
1
Sitr.comas
12
4
10
granulosa cell tumour (1) and teratoma ( 1 ) of the ovary osteochondrosarcoma
2
1
3
Mareh's disease
fi broleiomyoma of the oviduct (1)
(10)
Myeloid leucosis Nephroblastoma Hcpatic carcinoma
1 I
1
1
bacterial invasion, occurred in some skin sarconins. Most birds given a primary diagnosis of sarcomas had non-functional ovaries. doid LeucoAisTissues affected were kidneys (21), liver (17), ovary (15). skin (71, spleen ( 6 ) , muscle (4), mesentery (4), pleura (4),peritoneum ( 2 ) , intestine ( 2 ) and lung ( 1). Solid caseous yolks were found in birds with ovarian involvement, although similar lesions were also present in birds affected with ovarian abnormalities due to causes other than myeloid leucosis.
Mi
Prolapse m d Cunnibulisnz of the Vent Most birds with prolapse and cannibalism were i n good condition or were obese, were in pro-
duction and appeared to die from acute blood loss. Others had necrosis of the cloaca, and some of these had acute salpingitis. One per cent of birds with a primary diagnosis of prolapse and cannibalism had chronic salpingitis. Cage Layer Fatigue Birds diagnosed as having cage layer fatigue were dehydrated, and had greenish-white diarrhoea, brittle or broken bones, enlarged deformed costochondral junctions, haemorrhage into the tissues surrounding joints, and degenerating yolks in the ovary. Fntty Liver Syndrome Most birds that died of fatty liver syndrome had haemorrhaged severely from the liver into
TABLE 4 Tissue Distribution and Occurrence of Haemangiomas* Upper Alimentary and Respiratory Tract
Viscera ~~
I iver Kidney 0v'ir.l.
Me\enter) I unpc 5pleen Heart
740
Skin
122 54 25 18 It 11
8 8 1
(>vlducl
Infertine Totdl * Total number
Skeletal Muscles
~
~~~
4 Oesophagus 1 Pharynx and Larynx 8 Crop
258 of liens
H ifh
13
Muscles
32 32
Feet Body Legs Neck Wings
61 42
Vent
13 7
Face Comb and Wattles
37 23 17
5 205
haemangiomas - 211
Australian Veterinary Journal, Vol. 51. July, 1975
the abdominal cavity. There was evidence of previous ruptures of the liver in 7% of birds diagnosed as having fatty liver syndrome. Ninetysix per cent of birds with fatty liver syndrome were obese and were in production at the time of death. Histological lesions in the liver included widespread fatty change, multiple focal necrosis and haemorrhage. The macroscopic enlargement of the liver appeared to be due to a combination of intracellular fat deposition and haemorrhage. Starvation and Dehydration An arithmetical error made in the quantitative feed restriction program employed in flock B resulted in losses due to starvation and dehydration. The birds were emaciated, dehydrated, had hydropericardium, ascites, distended gall bladders and atrophied viscera, and were reluctant to walk or were recumbent. Miscellaneous Staphylococcus aureus was the organism most commonly isolated from birds with inflammation of the skin and from birds with arthritis and synovitis. Staph. aureus and Escherichia coli were isolated from birds with inflammation of the reproductive tract and viscera and from birds with nephritis. H. gallinarum was isolated from the trachea of 2 birds with respiratory disease. No viruses were detected in the trachea or caecal tonsil of birds with respiratory disease or from the kidneys of birds with nephritis and visceral gout. Discdon
Although strict comparisons between the prevalence of causes of morbidity and mortality in the 2 egg producing flocks are not valid in the absence of controls and replicates, some indication of trends can be gauged. The average weekly total of diseased birds in flock A (60.69) was greater than that in flock B (27.37). This resulted from a much higher incidence of leucoses and sarcomas and marginally greater losses due to prolapse and cannibalism, fatty liver syndrome and cage layer fatigue (Figures 1 and 2 ) . The prevalence of Marek‘s disease at different ages was similar in both flocks, and decreased markedly at 2 5 - 2 6 weeks of age. However, the prevalence of fatty liver syndrome at various ages differed between the 2 flocks. This could have been due to the different feeding programs used and may be related to reproductive maturity, as losses due to fatty liver syndrome increased in both flocks 10 - 12 weeks after 50% egg production was attained. Prolapse and cannibalism may also be correlated with reproductive maturity as it did not occur until birds were in lay. Austrulian Vereririnry Journal, Vol. 51. July, 1975
A similarity between the prevalence of lymphoid leucosis and haemangiomas at different ages was observed (Figure 3). Experimentally, the pathological response to leucoses and sarcoma viruses depends on the strain and dose of virus, the route of inoculation, the strain of bird and the age and sex of the bird (Purchase and Burmester 1972). Haemangiomas have been reproduced with a number of strains of leucosis virus (Purchase and Burrnester 1972), and recently Henderson et al (1974) incriminated an avian leucosis virus in field outbreaks of solid tumours, including haemangiomas. The histopathological variability of haemangiomas may be the reason for the existence of a number of synonyms for this tumour (Purchase and Burmester 1972). The high incidence of leucoses and sarcomas found in flock A was unexpected, as the high mortality of this strain of bird as pullets and in the first 6 months of lay was generally attributed to Marek‘s disease. Field and laboratory autopsy examinations of birds of this strain also suggested that fatty liver syndrome would be a more significant cause of loss in flock A. It is possible that the diagnosis of fatty liver syndrome had been confused on occasions, in previous examinations, with other causes of abdominal haemorrhage, particularly haemangiomas. The diagnosis of tumours of lymphoreticular cells was based on currently existing criteria (Purchase and Burmester 1972). Of these criteria, the finding of nerve lesions, the cellular morphology of tumours and the histopathological pattern of bursal tumours used separately or in combination were considered particularly useful in differentiating lymphoid leucosis and Marek’s disease. Bursal tumours occurred commonly in lymphoid leucosis, but infrequently in Marek’s disease. The bursal follicles were tumorous in lymphoid leucosis but cystic or necrotic in Marek‘s disease. Thickening of the bursal wall in those birds having bursal lesions of Marek’s disease was due to infiltration of lymphoreticular cells in the interfollicular septa. The adherent necrotic casts found in the lumen of some bursae appeared to result from cystic degeneration of bursal follicles causing accumulation of necrotic cellular debris. Bursal lesions, including cystic degeneration and necrosis of follicles, have been recorded in birds with experimentally reproduced Marek’s disease (Purchase and Biggs 1967; Purchase et a1 1968; Jakowski et a1 1969; Jakowski et a1 1970; Evans el ui 1971; Fletcher et al 1972). The tumours of lymphoid leucosis consisted mainly of large lymphoblasts which gave 341
the tumours a uniform, lightly basophilic appearance histologically. Marek‘s disease tumours were le5s uniform and more densely basophilic due to the pleomorphic cell population of small and medium lymphocytes, lymphoblasts, and plasma cells. These differential features were not readily detected once post-mortem decomposition had occurred. Xerve lesions in birds with Marek‘s disease were not found as frequently as expected. Goodchild ( 1969), in an extensive summary of nerve lesions in 502 field cases of classical Marek’s disease, found macroscopic neural lesions in almost 100% of birds. Purchase and Biggs ( 1967) reported that macroscopic nerve lesions were seen in SO% of chickens infected with isolates of acute Marek’s disease virus, although the frequency of occurrence of macroscopic nerve lesions in birds infected with an isolate of classical Marek’s disease virus was higher. One of the reasons for the apparent discrepancy between these results and those reported here could be the difficulty in evaluating autonomic nerve lesions in birds with extensive visceral tumours. particularly in the mesentery. The possibility that an agent other than Marek’s disease virus causes pleomorphic cell-type lymphomas in the viscera of adult hens cannot be overlooked. Macroscopic identification of tumours was digcult. This was particularly true with lymphoreticular cell turnours, sarcomas, myeloid leucosis, adenocarcinoma of the reproductive tract, granulosa cell tumours of the ovary and dysgerminomas of the ovary. Although some general indication of the tumour type could be obtained from the niacroscopic appearance and tissue distribution. it was concluded from this investigation that histopathological examination is required for accurate diagnosis of tumours. This could become particularly important in diagnosing tumours in birds vaccinated against Marek’s disease. Obesity has been incriminated as a contributing cause in fatty liver syndrome (Hofstad et a1 1972). In the investigation reported here, birds affected with fatty liver syndrome and prolapse and cannibalism appeared to have excess body fat. It is possible that a high incidence of disease in a flock due to these causes indicates that the laying flock as a whole is obese and may have inefficient feed conversion with respect to egg production. It was suspected that the peak Occurrence of cage layer fatigue in flock A at 41 - 45 weeks of age resulted from the settling out of the calciumphosphorous supplement added to the vegetable 31’
protein based ration. The possibility that the automatic auger feeding system and the coarseness of the mash assisted this sedimentation was considered likely. Excessively fluid faeces was a problem in flock A. Among the causes of “watery droppings” are lymphoid leucosis, cage layer fatigue and inflammation of the reproductive tract and viscera. The prevalence of these was higher in flock A than in flock B. Acute abdominal haemorrhage resulted mainly from fatty liver syndrome and haemangiomas, although less frequent causes were lymphoid leucosis, Marek’s disease, sarcomas and hepatic carcinomas. Blood clots in the oviduct were found in some birds with haemangiomas of the oviduct, abdominal haemorrhage and prolapse and cannibalism. This resulted in bloodstained eggs. The most common cause of visceral gout was chronic nephrosis and nephritis, other causes being tumours of the kidney, and tumours of the bursa of Fabricius or posterior peritoneal wall causing obstruction of the ureters. An upright posture and a “duck-walking” gait were features of birds with large tumours of the viscera, especially due to lymphoid leucosis, marked ascites, particularly in Marek’s disease, “egg-peritonitis”, and cystic oviduct. Paralysis and ataxia were seen in birds affected with Marek‘s disease, cage layer fatigue, tumours of the kidneys, leg muscles, shanks or feet, trauma and fracture of limbs, arthritis and synovitis and general debility. Abnormalities of the head and neck posture, such as torticollis, kyphosis and tremour, occurred due to brain lesions of Marek’s disease, medulloblastoma and astrocytoma, and in middle ear infection. Summary
Laboratory examination of all birds that were culled or died during an eight-month period in two commercial laying flocks was performed to reveal the causes of disease and their prevalence. The average weekly total of diseased birds was greater in one flock (60.69) than the other (27.37). This resulted mainly from a high incidence in the former flock of leucoses and sarcomas, although losses due to fatty liver syndrome, prolapse and cannibalism and cage layer fatigue were also marginally greater in this flock than the second. Haemangiomas occurred more frequently in the flock with the higher disease level. A total of 273 hens of the 2,000 examined from this flock had single or multiple haemangiomas. Special features of the major causes of disease were outlined and discussed. Australian Veterinury Journal, Vol. 51. July, 1975
A conclusion made from this study was that histopathological examination is necessary for accurate diagnosis of avian tumours. Referencm Campbell, J. G. (1969) -“Tumours of the Fowl”. 1st ed, William Heinemann Medical Books Limited, London. Evans, D. L., Beasley, J. N. and Patterson, L. T. (1971) - A v i a n Dis. 15:. 680. ._._ Fletcher, O . J . , Eidson, C. S. and Kleven, S. H. (1972) -Avian Dis. 16: 153, Goodchild. W. M. (1969) - V e t . Rec. 84: 87. Henderson, B. E., Gardner, M. B., Charman, H. P., Johnson, E. Y., Rucio, T., Sarma, P., Alena, B. and Huebner, R. J. (1974) -Avian Dis. 18: 58.
Hofstad, M. S., Calnek, B. W., Helmboldt, C. F., Reid, W. M., Yoder, H. W. (1972) “Diseases of Poultry”. 6th ed, Iowa State University Press, Ames. Jakowski, R. M., Fredrickson, T. W., Chomiak, T. W. and Luginbuhl, R. E. (1970) -Avian Dis. 14: 374. Jakowski, R. M., Fredrickson, T. W., Luginbuhl, R. E. and Helmboldt, C. F. (1969) --Avian Dis. 13: 215. Jordan, F. T. (1956) -J. comp. Path. 66: 197. Purchase, H. G . and Biggs, P. M. (1967) -Res. vet. Sci. 8 : 440. Purchase, H. G. and Burmester, B. (1972) -In “Diseases of Poultry”. Ed. by M. S. Hofstad, 6th edn, Iowa State University Press, Ames. Purchase, H. G., Chubb, R. C. and Biggs, P. M. (1968) -J . natn. Cancer Inst. 40: 583. Rosenfeld, Lorraine E. (1971) Aust. vet. J . 47: 492. (Received for publication 10 July 1974)
-
-
BOOK REVIEW THE PRINCIPLES OF HORSESHOEING ‘Horseshoeing’, Anton Lungwitz is quoted as having written at the turn of the twentieth century, ‘is an industry which requires, in equal degree, knowledge and skill.’ Butler’s excellent text* will go far in assisting those interested in attaining at least the first of these requirements. The author suggests, in his first chapter, that the number of horses in the United States of America after a low of 3,000,000 in 1960 will reach 16,000,000. by. 1980. This increasing popularity of horses, which IS probably common to many developed countries, is just one indication of the need for an up-to-date manual o n this ancient art. The subject matter covers many aspects of the horse’s hoof and its maintenance, including an interesting introduction describing some of the superstitions and folk-lore surrounding farriers and their craft. Written by an obviously dedicated expert, the chapters include the anatomy of the hoof, horse handling and forge techniques; the latter subject being dealt with quite extensively. The notes on corrective shoeing are presented *The Principles of Horseshoeing. Dou Butler. Published by Doug Butler, 1611 East Shore Drive, fthaca, NY, USA, 1974 Pp. 428 $19.95.
Australicin Ve/erinary Journal, Vol. 5 1. July, 1975
logically and are well illustrated; they should be valuable for the veterinarian searching for the correct types of shoe to use in the treatment of various hoof and leg conditions. The author has managed fairly well to bridge the gap between horseman and veterinarian in this area of treatment, without arming the layman with too much potentially ‘dangerous’ pharmacological knowledge. A strong feature of the book is the methodical clearcut layout, with each subject clearly defined and presented in an easily followed form. The diagrams are excellent and are used to great advantage. Likewise, the photographs are of good quality and add to the readability of the text. The index is refreshingly comprehensive - nowadays indexes can be more frustrating than helpful! A helpful list of general references is given. This is a good functional book, and, although unfortunately fairly expensive, is well worth the consideration of those who require an extensive knowledge of the horse’s hoof, as well as those looking for a practical manual of horseshoeing. C. D. Mackenzie
343
