A ColourAtlas of

Diseases of the
Domestic Fowl
&Turkey
C.J.Randall
MA VetMBMRCVS
Ministry of Agriculture. Fisheries and Food
Veterinary Laboratory.
Eskgrove. Lasswade.
Midlothian.
Scotland.

Wolfe Medical Publications Ltd

Published by
IOWA STATE UNIVERSITY PRESS
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U.S., Canadian, and South American rights

ISBN 0-8138-0353-5

(f;) Crown copyright 1985

Published by permission of the
Controller of Her Majesty's Stationery Office
Published by Wolfe Medical Publications Ltd 1985
Reprinted 1986
Pri nted by W. S.Cowcll Ltd, 8 Buttermarket, Ipswich,
England
ISBN 0 7234 0827 0
For a full list of Wolfe Veterinary Colour Atlases, plus
forthcoming titles, please write to Wolfe Medical
Publications Ltd, Wolfe House, 3 Conway Street, London
WlP6HE

All rights r eserved. The contents of this book, both photographic and
textual, may not be reproduced in any form, by print, photoprint,
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Contents
Acknowledgements 5
Preface 7
Bacterial diseases
Coli bacillosis (including peritonitis in layers and salpingitis) 9
Fowl cholera 13
Yolk sac infection and omphalitis 16
Staphyloccocal infection 18
Necrotic enteritis 20
Gangrenous dermatitis 22
Listeriosis 23
Erysipelas 24
Tuberculosis 25
Vibrion ic hepatitis 27
Salmonellosis 27
M ycoplasmosis 30

Viral diseases
Infectious bursal disease (Gumboro disease) 34
Inclusion body hepatitis 36
I laermmhagic enteritis in turkeys 37
Fowl pox 38
Infectious laryngotracheitis (I LT) 39
Newcastle disease 40
Infectious bronchitis 42
Egg drop syndrome '76 ( 127 adenovirus/BC 14 infection) +l
Infectious avian encephalomyelitis (epidemic tremor) 44
Viral arthritis and tenosynovitis 46
Marek's disease (including transient paralysis) 47
Lymphoid leukosis and other leukoses 52
Lymphoproliferati ve disease of turkeys 57
Reticuloendothcliosis virus induced tumours in turkeys 58

Other neoplasias
Adenocarcinoma of the reproductive tract of the hen 59
Leiomyoma of the oviduct Iigaments 60
Squamous cell carcinoma of the skin 60

Fungal diseases
Aspergi llosis 61
Dacrylariosis 63
Candidiasis (~
Parasitic diseases
Ascaridiasis 65
Capillariasis 65
Coccidiosis 65
Histomoniasis 70
Cryptosporidiosis 70
Scaly leg 71
Lice 71
Red mite 71
orthcm fowl mite 72

Nutritional deficiencies and metabolic disorders

Riboflavin deficiency 73
Encephalomalacia (crazy chick disease) 74
Rickets 75
Calcium deficiency in adult laying fowl 77
Fatty liver and kidney syndrome 78

Diseases of uncertain or unknown aetiology

Fatty liver haemorrhagic syndrome in laying fowl 81
Sudden death syndrome in broilers ("acute heart failure .. ·nip-over') 83
Sudden death syndrome in adult laying fowl 84
Cardiohepatic syndrome in turkey poults ("hepatosis' ) 85
Ascites and congestive heart failure in broilers 86
Round heart disease 88
Dyschondroplasia 89
Valgus leg deformity in broilers ('twisted leg·) 91
Twisted leg in turkeys 93
Renal fai lure (visceral gout) 93
Stunting syndrome of broi lers (malabsorption) 97
Acute pectoral myopathy of broiler breeders 100

Miscellaneous conditions
Spondylolisthesis (kinky back) 102
Ruptured gastrocnemius tendon 103
Deep pectoral myopathy 103
Plantar pododermatitis 106
Moult 106
Persistent right oviduct 107
Internal layer 107
Prolapse of the oviduct 108
Cannibalism 108
Poor thriving in chicks and poults 108

Index 11 3-1 I()

 Acknowledgements
I am very grateful to both past and present colleagues for
discussions about many aspectsofpoultrydisease.ln panicular
I thank J F Harbourne . C T McCrea. A R Hunter. J W
Macdonald and Helen G R Jones. Much useful advice on the
draft manuscript was given by Mr J W Macdonald. lasswade
laboratory. Dr M Pattison. Sun Valley Poultry Ltd. Dr l
Payne. Houghton Poultry Research Station. and Drs W G Siller
and P A L Wight. Agricultural Research Council. Poultry
Research Centre. I am most grateful fortheirhelp. Dr J GRoss.
Director. Lasswade Laboratory, is thanked for giving con-
tinuous suppon and sympathetic encouragement throughout.
I am indebted to the following for providing me with
valuable transparencies: the late Dr J E Wilson. previously
Director of the Lass wade Laboratory, for 63-67, 96, 138. 149.
176, 191 and 247 , Dr R C Jones , Sub-Depanmem of Avian
Medicine , UniversityofLiverpool. for 120-123 (copyrighl for
these four pictures rests with Dr R C Jones), and to Mr D E
Gray. Librarian at the Central Veterinary Laboratory. for
arranging the loan of 48, 68-70, 85.98, 99. 102 and 103 from
the Library· s collection. I also thank Mr Gray for undertaking
the task of preparing the Index. Sections of reticulocndothc-
liosis virus-induced tumours in turkeys and round heart in the
fowl were kindly provided. respectively. by Dr J S McDougall.
Houghton Poultry Research Station and by Dr C Riddell.
Western College of Veterinary \1edicine. University of
Saskatchewan.
The tjssue sections phorographed were prepared by the staff
of the Pathology section at Lasswade who are thanked for
dealing expertly with many requests. Mr W Gordon. ably
assisted by MrS Lees. Miss S \1 Clark and Mrs E .\ltelvin.
helped at all stages with the photography. I am indebted to them
for their enthusiasm and skill . Mrs L Johnstone is thanked for
cheerfully typing the text.
 Preface
The purpose of this atlas is to provide the diagnostician with
photographs of the main post-mortem and histopathological
features of common diseases in the domestic fowl and turkey.
The atlas does not aim to coverthe other procedures that may be
required to confirm a diagnosis. The text has been kept to a
minimum and is intended to be read in conjunction with
textbooks of poultry disease (sec page Ill ).
Selection of conditions reflects the aurhor·s experience in
Great Britain. Inevitably this has led to the omission of some
diseases of interest but photographs of less frequently seen
disorders are included where they have been thought appropri-
ate . In the main. the photographs have been assembled during
the last ten years; diagnostically they span a period of seventeen
years.
Diseases that might be usefully considered together are
arranged under main group headings rather than being listed
alphabetically. A miscellaneous group of conditions, whose
aetiologies are generally understood, is listed separately from
those of uncertain or unknown cause. Names have been
selected for some conditions (236-246) that are seen as distinct
entities but which still require further definition.
All photomicrographs are of tissue sections stained with
haematoxylin and eosin unless stated otherwise. In two in-
stances sections from species otherthan the fowl and turkey are
shown. Water olublc acrylic resins have been used occasion-
ally for tissue embedding to show particular features and this
use is also indicated in the legends. Magnifications of photo-
micrographs have been omined a<; these were thought to be of
doubtful Yalue.
 Bacterial Diseases

Coli bacillosis
.:1 luding peritonitis in layers and salpingitis)
1
,, cpticaemia. Escherichia coli
....._ mg evere pericarditis, perihcpa-
...nd air sacculitis in a broiler
, mg a primary viral infection of
-e--piratory tract. T he fibrinous
ze covering one lobe of the liver
~n cut to show the surf~ce of the
=~beneath . Hepatic and pericar-
.e ions of this type are occa-
...::~ seen in some systemic sal-
ella infections in young chickens
... rkeys (see 59).

2
: C j septicaemia. Liver section
mg the fibrinous nature of the
It on the surface of the organ.
-;: a scarlet blue.

9
-
3 Coli septicaemia. Eosinophilic
coagulum in a periarteriolar sheath in
the spleen. This feature is frequently
encountered in cases of Coli septi-
caemia. It is usually marked in this
infection but similar changes may
occur in other septicaemias and
viraemias.

4 Coli septicaemia. Synovitis of

hock joints is commonly found in
broilers. Creamish coloured exudate
tends to be tinged with brown. There
may be concurrent lesions of
osteomyelitis. particularly at the pro-
ximal tibiotarsal growth plate (see
31).

5
5 Coli septicaemia. Salpingitis in a
3-wcck-old broiler. Inflammation of
the immature oviduct is a relatively
common finding in broiler~.

10
 6
Coli septicaemia. Turkey grower.
....e~ions were confined in rhis instance
an overall carcase congestion and a
""!larked congestion of the spleen
.u-row). This bird gave a serological-
:· positive reaction for Mycoplasma
~eleagridis antibodies.ln this species
~ricarditis may accompany Coli sep-
. ..:aemia but fibrinous deposits on the
cr are less common. Greening of
'1e liver may take place after expo-
ure tO the air.

7
- E. coli is isolated from the great
...~1ority of cases of peritonitis in
-ult laying fowl. The condition is
·en termed 'egg peritonitis'. but the
-e,encc of yolk mixed with the ex-
.......te is variable . Birds dying in acute
:..ge arc usually septicaemic.

8
!...aying fowl may die as a result of
-.wte salpingitis. Many survive this
- ,ode, with the result that the in-
mmatory exudate becomes panial-
~ganised. The affec ted oviducts
-. be extremely enlarged and
•• .JPY most of the abdominal cavity.
>li is usually isolated from these
')OS .

II
9 The exudate contained within the
oviduct of 8 has been cut to show the
onion-layered texture of the in-
flammatory exudate and, in this case,
a shelled egg.

10
10 Layering of fibrinous exudate
within an oviduct. Martius scarlet
blue.

11 Coli granuloma (Hjarres disease)

affecting the caeca of a laying fowl.
The lesions must be distinguished
from those of tuberculosis. which is
best done histological !y (see 53) .

11

l2
12 Coli granuloma. Cross section of
a granuloma from 11.

Fowl cholera (PriSfeurella multocida)

13
13 Swollen wattles in a male broiler
-eeder due toP. mu/tocida infection.
:be affected males may be slightly
.;.epresscd in localised infection of
~ type. Swollen wattles may also
... cur amongst the females, as well as
- ~ell ulitis, which is usually seen over
-e head and neck.

- Core of pus in a swollen wanleof a

.ler breeder hen. P. mulrocida can
-c ,oJatcd from most acute lesions of
'type but only rarely from chronic
- -C'ises. This may give rise to
'":le diagnostic difficulty as wattle
... e scs can be caused by a variety
- ..cteria.

13
15 16

17
15 Purulent synovitis in a hock joint
of an adult broiler breeder cockerel.
Lameness may be a presenting clini-
cal sign in some outbreaks.

16 Comparison of pale flecked ex-

udate (right) from a case ofstaphyloc-
cal synovitis with the more yellow-
tinged granular exudate obtained
from a P. multocida infected joint.

17 Peritonitis is often found in adult

layers in septicaemic fom1S of the
infection.

18
18 Blood stained mucus in the mouth
of a septicaemic turkey breeder.

14
19 Purulent pleuropneumonia in a
I0-week -old turkey grower. This bird
was unvaccinated. Pneumonic le-
sions are more commonly seen in the
rurkey than in the fowl.

20 \1asses of pasteurellas within a

_ng of a turkey that died from a dual
..:::fection of P. multocida and New-
-~rle disease.

~. Acute pneumonia in a 22-week-

- broiler breeder. Pasteurellas
,_Jy stain more basophilically
-7Cl\\) in H & E preparations than
-~ other commonly encountered
- --::1-negativc organisms. The tissue
:.=right ofthe bacte1ia is necrotic,
~ lhe left is reactive.

15
 Yolk sac infection 22
and omphalitis

22 The abdomen of this chick is great Iy distended as a result of

yolk sac infection. Most birds die at 3-4 days of age. There may
be an accompanying omphalitis. The carcasses often smell
unpleasant(y.

23
23 Intense inflammation of an in-
fected yolk sac.

24
24 The normal consistency of the
yolk is lost and in the acute stages of
the disease the contents are thin and
have a strong odour. The presence of
soft and friable viscera together with
moist abdominal skin and down led to
the condition being called .. mushy
chick disease' ' .

16
 25
25 The contents of the infected yolk
sac may become inspissated if the
chick or poult survives into the second
week of life. Infected yolk sac rem-
nants containing deeply pigmented
cheesy material are a frequent in-
cidental post-mortem finding in older
birds.

26
16 Intense lung congestion (arrow)
occurs in the acute stages. Note the
9001 of yolky material within the
abdominal cavity.

27
:- A wide variety of bacteria may be isolated either in
:.1gle or mixed infections. E. coli is frequently cultured
"TOm affected birds and may lead to classical lesions of
~nli scpticaem ia (see 1) towards the end of the first week.
S:11ovitis and osteomyelitis can also be seen in coliform
~ other infections introduced by this route.

17
Staphylococcal infection (Staphvlococcus aureus)

28
28 Synovitis associated with staphy-
loccocal infection in a 10-week-old
broiler breeder. This infection is most
often seen during the rearing period.
The base of the gastrocnemius tendon
is usually swollen as well as the joint.
Reoviruses may need to be consi-
dered as primary infecting agents in
some outbreaks (sf!e 120-123).

29
29 The hock joint in 28 has been
opened to show the large quantity of
purulent exudate. This lesion often
extends into the sheaths of the digital
flexor tendons and the gastrocnemius
tendon.

30 31
30 Chronic case of staphylococcal
arthritis in a young broi ler breeder
showing erosion of the carti lage over
the distal tibiotarsal condyles.

31 Osteomyelitis in a turkey grower.

The infected tissue is pale and crum-
bly and situated distal to the proximal
growth plate of the tibiotarsus.
Osteomyelitis is frequently found at
this site in broiler types and turkey
growers. Staphylococci (and E. coli)
are often isolated from such lesions.
The long bones - particularly the
tibiotarsus - should always be split
when young birds are presented with a
history of lameness.

18
 32
32 Osteomyelitis. A small in-
tlammatory focus in a tibiotarsal
growth plate containing numerous
clusters of bacteria.

33 Clearly defined necrotic lesions in the liver of a

~ 5-week-old turkey breeder that had been de-beaked I0
days previous!y. There were concurrent lesions of syno-
itis. Hepatic lesions of this type are commonly seen in
•.!Ying fowl in association with vegetative endocarditis.
- ;.aphylococcal septicaemias occur from time to time in
~ommercial and breeding hens with few lesions other
:.'!an generalised carcase and hepatic congestion .

34
J..t Livcrlesionssimilarto those in 33
ften show a few scattered colonies of
Gram-positive cocci sutToundcd by
.age 7.ones of necrosis and with
~le innammatol)· reaction at the
-xriphery. Gram.

19
35 Sporadic deaths, particularly in
commercial layers, are often caused
by vegetative endocarditis of the left
atrio-ventricular valve. Streptococci
may also be isolated from vegetative
lesions of this type.

Necrotic enteritis
36 Early necrotic enteritis in the
small intestine of a 3-week-old broil-
cr. The mucosal surface is abnomtal-
ly pale due to necrosis of the tips of the
villi.

37 Advanced lesion. The necrotic

mucous membrane is fissu red and de-
taching from the deeper layers.
Sloughing of parts of the mucous
me mbrane may give the serous sur-
race a faintly speckled appearance.
Most of the upper small intestine is
usually involved in the lesion. The
condition is seen predominantly in
young broilers and broiler breeders
(see 1S9).

20
 38
38 Smear of small intestinal contents
showing the predominance of Gram-
positive bacilli. The~e organisms arc ..
'\\ •
a
often decaying and stain variably.
Profuse growths of Clostridium per-
f ringem are isolated from intestines of
birds that have died. Gram. .,
....•
', _, -

39 Necrosis of the inn~r par1 (arrows)

of the small intestinal mucosa.

.$0
.W This s~ction has b~en stained by
:.he Gram-Weigart method. Numer-
~u Gram-positive organisms are
1 ·ible on the inner surface of the
necrotic mucosa (right). The p ink line
:J.rrows)represents th~ junction of the
:_1ner necrotic tissue from the still
• rablc deeper mucosa.

21
 41
41 Kidneys of birds that have died as
a result of necrotic enteritis are usual-
ly pale. This feature is often encoun-
tered in bacterial septicaemias and
toxaemias and may give rise to the
false impression that primary renal
disease is present. Histologically.
few changes are seen other than mild
dilation of the distal parts of nephrons
which is interpreted as a tenninal dys-
function with, possibly, urates col-
lecting in the distal tubules.

42
42 Intense congestion of a broiler
liver. This degree of congestion is
typical of acute cases. In some in-
stances clostridia invade the portal
blood system post mortem with the
result that auto!ysis is more advanced
in the tissue surrounding the in-
trahepatic veins, which causes
mottling.

Gangrenous dermatitis
43 A small area of wet inOamcd skin 43
is present on this broiler's wing. Le-
sions like this are variable in size and
may be present anywhere on the
body. The condition is usually associ-
ated with either single or mixed infec-
tions of coagulase positive staphylo-
cocci and clostridia (eg C/. septicum '
and C/. perfringens). During the early
part of an outbreak birds may die
without obvious lesions affecting the
skin but in some instances small wet
sores can be found between the toes.
Birds arc rarely seen ill. If clostridia
are involved the rate of decomposi-
tion of carcasses may be very rapid
with the result that 'green' carca-;ses
can be submitted with the history that
the birds have been picked up as fresh-
ly dead an hour or two beforehand.
22
 44
44 The skin lesions defcather very
easily and are usually underrun with
gelatinous and sanguinous fluid.

45 Pru1 or all of the lung may undergo

liquefaction. This is particularly
common when the infection is pre-
dominantly staphylococcal. It may be
the most notable post-mortem feature
of carcasses examined at the begin-
ning of outbreaks. Kote the small
unaffected areas of tissue at either
end.

46 Clumps of staphylococci in a
necrotic zone of lung.

Listeriosis (LisTeria J/10110(\"/0genes)

~7
~7 Myocarditis in a 7-week-old commercial layer pullet. The
heart has been cut through to show almost complete replace-
ment of the myocardium with pale inflammatOry tissue. Focal
lesions may occur. The condition is uncommon and should not
he confused with lymphoprolifcrative lesions of Marek's dis-
ease that often affect the heart. this is par1icularly so when
necrosis has occurred in the lymphoid !llmour giving rise to
yellowish foci within the neoplasm.

23
 48
Erysipelas
(Erysipelmhrix rhusiopathiae)

48 T he condition is common in tur-

keys but rare in the fowl. Carcasses
are congested and show general septi-
caemic changes . The head of this bird
is scabbed. Gram-stained smears of
tbe liver, kidney and bone marrow
can be useful diagnostically if treat-
ment has to be started immediately . In
smears from tissue, the short rods
tend to be more robust and strongly
Gram-positive when compared to
those made from cultures.

49 The livers of affected turkeys may

have a distinctive pur-boiled appear-
ance.

50
50 A clump of E. rlwsiopathiae in a
sinusoid of the liver shown in 49. The
sinusoidal disruption is partly artifac-
tual. Aery Iic resin.

24
Tuberculosis (Mycobacreriwn avium)

51
51 The disease is common in free
range fowl but is only rarely seen
under intensive systems of husban-
dry. Affected birds gradually become
emaciated. Yellowish caseous
nodules are most commonly found in
the liver, spleen and intestine. Well
developed lesions in rhe liver can
usually be shelled out from the sur-
rounding parenchyma.

52
52 A pale granuloma within the mar-
row cavity of a femur. Lameness
often occurs in affected birds due to
the development of such lesions. par-
ticularly at the di ·tal end of the femur.

53 Large numbers o f acid fast bacilli

arc present in smears from most avian
lesions. Smears are best made by
crushing individual nodules between
two g lass s lides. Z ich l-Ncclson.

25
54 Developing tubercle in liver of
hen. At this stage the central part of
thelesionismainlycomposedofpale-
staining epithelioid cells.

55 A more advanced lesion in which

central necrosis has taken place.
Giant cells are starting to pallisade
round the necrotic zone. Numerous
macrophages are present peripheral-
ly. Connective .tissue encapsulation
has not yet occurred.

56 A large mass of granulation tissue

was present at the thoracic inlet of a
commercial layer. Many giant cells
were scattered through the lesion in
which there was considerable deposi-
tion of amyloid. A giant cell is seen
engulfing an amyloid focus .

26
 57
57 A Congo Red stain on the tissue in
56 demonstrates the characteristic ap-
ple-green birefringence of amyloid
under polarised light.

58
Vibrionic hepatitis
58 This condition is now rare and when seen is usually in
young pullets. The liver may be enlarged and friable.
Numerous small pale lesions are seen here under the
capsule of a discoloured liver.

Salmonellosis
59
This section refers only to diseased
birds. Many birds may be infected
with salmonellas and show no clinical
or post-mortem signs. As used here.
the tem1 'salmonellosis· also refers to
the now rare diseases caused by Sal-
ltWnella pullorwn and S. gallinarum.

59 Salmonella typhimurium. Gross

lesions are very variable. Heavy mor-
tality may result in young chicks and
turkey poults. Focal lesion are pre-
sent in the liver of this 7-day-old
broiler. In birds of a few weeks of age
the gross lesions may occasionally
resemble those of Coli septicaemia
(see 1) . Histologically. diagnoses of
meningitis are made from time to time
in young chicks with clinical histories
of nervous signs.

27
60 61

62
60 S. typhimurium. A section of liver
from 59.'Necrotic tissue in one of the
focal lesions is in the lower part of the
photograph and is staining more cosi-
nophilicaliy than the unaffected
hepatocytcs above.

61 S. t)]Jhimurium. Vermiformappearanceofthecaecarcsult-
ing from an acute typhlitis in a 7-day-old broiler. The presence
of this lesion is variable but salmonella infection should be
suspected when it is seen.

62 S. t)phimurium. Cheesy cores of inflammatory debris

within the caeca of a boiler chick.

63 S. gallinarum (fowl typhoid). In most acute cases the lungs

show a brown discolouration.
63

28
64 S. gallinarum. The carcases of birds that have
died from the acute disease are jaundiced and the
liver shows a characteristic bronzing (right) after
exposure to the air. Note also the se\'ere conges-
tion of the spleen.

65 S. pul/omm (bacillary white di-

arrhoea). Greyish-white necrotic foci
in chick lung. Similar lesions may be
present in the hcan and liver.

66 S. pullonmt. Synoviti of hock

joints in chicks.

29
 67
67 S.pullorum. In adults, the ovary is
the organ most frequently involved.
This specimen shows a few degener-
ate ova, some of which are attached to
the body of the organ by long stalks .
The contents of the affected ova are
discoloured and may be inspissated.

Mycoplasmosis
68 69

70
68 M. gallisepticum. Swelling of the infra-
orbital sinuses in a turkey.

69 M. gallisepticum. Infra-orbital sinus of a

turkey opened to show sticky exudate in an
acute case.

70 M. ga1lisepticum. Gross lesions tend to be

more pronounced in the turkey and infection is
often accompanied by air sacculitis (yellow
pointer) and pneumonia.

30
71 M. gal/iseptic.wn. Pneumonia
associated with infection in a turkey.
The inflammatory exudate is mixed.

72 M. synoriae (infectious synovi-

tis). Subcutaneous bursitis over the
sternum in a 9-wcck-old commercial
layer pullet. Note the loss of condi-
tion (NR M. l:nwviae may be associ-
ated with respiratory disea. c corn-
picxes in broilers: joint and bursal
lesions in such nocks are usually
absent .)

73 M. syno1·iae. Two swolkn fompads (centre and left)

ofhroilers. This feature may be ,·ery pronounced. There
is frequently swelling of the hock and main wing joints.
As in other mycopla ma infections. egg transmission
occurs and the diagnosis hould be carefully confirmed .
both serologically and culturally.

74 M . SYIIOI'iae. Footpad exudate in an acute infection of

a commercial layer. The exudare is characteristically
glairy and tenacious.

74

31
75 76

77
75 M. synoviae. Chronic lesions in a
footpad of a commercial layer. In
chronically inflamed footpads and
joints the exudate is often a deep
orange-yellow colour.

76 M. synoviae. An inflamed wing

joint has been opened to demonstrate
the exudate. Inflammation of wing
joints is occasionally seen in staphy-
lococcal infections but infectious
synovitis should always be suspected
when lesions are being encountered
frequently in this joint and accompa-
nied by sternal bursitis.

77 M. synoviae. Purulent exudate to

the right of a chronically inflamed 78
synovial membrane.

78 M . meleagridis. Infection may

cause poor growth and feathering,
chondrodystrophy. air sacculitis and
diarrhoea(turkeysyndrome '65). The
legs of this turkey have a severe varus
defom1ity at the hock joint.

32
79

79 M. meleaxridis. Closer view of a chondrodystrophic

tarso-metatarsus in the same bird as shown in 78. Note
the shortening and flattening of the proximal head.

80 M. meleagridis. Flecks of caseous exudate within the

abdominal air sacs of a 6-week-old turkey.

81 M. meleagridis. Section of a widened head of an

affected tarsometatarsus. Martiu. scarlet blue.

82 M. meleagridis. Paucity of developing chondrocytes

with some necrosis (arrows) in !:he transitional zone of
the growth plate seen in 81 . Marti us scarlet blue.
 Viral diseases

Infectious bursal disease

(Gumboro disease)

83 The bursa of Fabricius is slightly

swollen in this 3-week-old broiler.
The small highlight on the surface has
been produced by a thin layer of gela-
tinous oedema covering the serous
surface. This infection was sub-
clinical.

84 Swollen bursa of Fabricius in a

clinical case.

85 Haemorrhagic lesions arc usually

encountered in the bursa i{ mortality
is occurring. Lesions vary in severity
from a few petechial haemorrhages
on the plicae to very severe haemor-
rhage. as here. throughout the organ.
Purulent luminal exudate may be-
come inspissated . The kidneys of
birds that have died are often swollen
and pale. This is caused by a terminal
dysfunction and is not a nephritis.

34
86 Extensive haemorrhages arc pre-
sent in the follicles and interfollicular
tissue. Purulent exudate (arrow) has
collected in the bursal lumen.

S7
87 Sub-clinical disease. Bursal
haemorrhages are not usually present
but a higher power view of an injured
follicle shows lymphocytolysis and
heterophilic infiltration. Infectious
bursal disease must be distinguished
histologically from cause~ of 1I011-
i11jlammarory lymphoid depletion and
premature bursal regression. This is
readily done providing the lesion are •
observed during the early stages of the •
disease when the acute inflammatory
reaction is evident.

88 Cystic spaces forming in injured folli-

cles . T his may be a prominent feature during
resolution. The acute inflammatory reac-
tion is quickly cleared in most cases leaving
severely depleted follicles and fibroplasia of
the interfollieular connective tissue. Hyper-
plasia of the bursal epithelium is often
marked at this stage.

35
 89
89 Small linear muscular haemor-
rhages may be present in birds that
have died. Although the pectoral
muscles are shown here, the outer
surface of the thigh is the site where
these lesions are most likely to occur.

Inclusion body hepatitis

90 The disease "is seen mainly in young broilers

and broiler breeders. The carcases are usually
congested and the livers may show characteristic
small speckled haemorrhages throughout the sub-
stance of the organ. In some cases, however, the
liver may be just swollen and pale. Gross lesions
may need to be distinguished from those of the
fatty liver kidney syndrome (see 216-224) .

91 The appearance of intranuclear

inclusions within hepatocytes is vari-
able. In some cases these may be
almost entirely eosinophilic and well
haloed or they may be predominantly
basophilic and solid. If the lesions are
focal, inclusions tend to be seen near
their periphery.

36
92 The kidneys arc often congested
and tinged a muddy yellow colour,
possibly due to slight carcasc
jaundice.

Haemorrhagic enteritis in turkeys

93 The small intestine is usual ly dis-
tended with blood and mucosal de-
bris . The mucosa. particularly in the
upper region. tends to have a velvety
appearance. The spleens may be
swollen and mottled.

94 The presence of intranuclear in-

clusions (solid , pale-staining bodies
arc arrowed) with in the inrestinal
lamina propria is a useful diagnostic
feature. Acrylic resin.

37
95 Numerous. similarly staining in-
tranuclear inclusions {arrows) within
the reticulum cells are visible in the
spleen. Acrylic resin.

Fowl pox
96
96 The disease may affect both
chickens and turkeys and can cause
cutaneous and internal lesions. Here.
pox lesions are present in the oro-
pharynx of a hen. Lesions may also
occur in the trachea and s hould be
distinguished culturally and his-
tophathologically from di phtheritic
forms of ILT (see 99). The disease is
now seen ·infrequently but ha
appeared in some battery systems .
both on its own and in combination
with other infectious agents.

97 Large eosi nophil ic cyto plasmic

inclusions in a prolife rative epithel ial
lesion. Pigeon skin is shO\m here in
order to demonstrate the typical avian
pox le ion.

38
Infectious laryngotracheitis (ILT)
98
98 Lesions are confined to the re-
spiratory tract. Post-mortem ex-
amination may show occlusion of the
tracheal lumen with blood and blood
clots.

99
99 In more chronic forms of the dis-
case there may be a pronounced
diphtheresis in the trachea.

100
100 Two partl y fixed broilerrrachcas
are compared. The one on the right is
full of purulent debris. the other con-
tains a hlood clot.

39
101 Eosinophilic intranuclear inclusions are present in a
clump of epithelial cells that have been sloughed from the
inflamed mucous membrane. These were lying in a large mass
of inflammatory exudate within the lumen. Such clumps of
cells may be quite small but often repay close examination. The
inclusions may not necessarily be haloed and can therefore be
more difficult to see. If groups of nuclei containing haloed
inclusions are packed close together the margination of the
chromatin can give a 'wire-netting' effect.

Newcastle disease
102 Depending on the strain of v irus
and its tissue tropism the post-mortem
findings are very variable. Petechial
haemorrhages are shown here on the
heatt and abdominal fat in a congested
carcasc of a fowl. Haemorrhages on
the tracheal mucosa and air sacculi tis
may be seen with some pneumotropic
strains of the virus.

I 03 lf present, proventricular
haemorrhages are usually seen on the
sutface of the papillae and can be
distributed in a ring near the j unction
with the gizzard. Haemorrhagic le-
sions may also be found in the intes-
tine, particularly on the sutface of the
caecal 'tonsils'.

40
 104
104 Submucosal oedema (arrow) in
the trachea of an unvaccinated fowl.
Inflammation has resulted in most of
the epithelium being shed, leaving
small protmding pegs of tunica pro-
pria. The lesion is not specific but was
observed duri ng outbreaks involving
a pneumotropic strain ofthe virus.

105
105 Non-pumlcnt encephalitis may
be present. In this photograph local-
,'\
ised g liosis (arrows) involves the .... :;
molecular layer of the cerebellum in a
fowl.
.,:.
... I
I.

'
.\

106 Perivascular cuffing in a section

of cerebrum from a fowl.
;

11. "'tr ""'.,

" t~
;Jir•v 1>0

¥I ~· # ....

.. ~.. •

41
Infectious bronchitis
107
107 Acute tracheitis in a broiler.
Secondary E. coli infection is estab-
lished. Tracheal inflammation may
vary from diffuse intlammation to a
barely perceptible increase in produc-
tion of a watery mucus. Gross lesions
are occasionally confined to the bron-
chi and obstruction of these with in-
spissated inflammatory exudate may
result in asphyxiation of the bird.

108
108 A dense lymphocytic infiltration
is present in the tracheal mucosa of an
unvaccinated 6-week-old broiler
breeder. This type of lesion is often
seen in field cases but is of doubtful
specificity.

109
109 Acute nephritis in an unvaccin-
ated 6-week-old broiler breeder. In-
fectious bronchitis virus was isolated
from this tissue.

42
 110
110 Interstitial nephritis produced in
an experimental challenge of pre-
viously unvaccinated 10-week-old
fowls with the H52 strain of the virus .
This lesion was characterised by
heavy mononuclear infiltration in
which large numbers of plasma cells
were present . Some plasma cells con-
tain periodic acid schiff (PAS)-
positive Russell bodies. PAS-
hacmatoxylin.

111
111 A wide range of egg abnorrnali-
ties may be observed if susceptible
laying fowl are infected . Shells are
often ridged or have concretions on
their surface.ln others. as here. shells
may be misshapen in other ways.

112
112 ·rh~ int~mal q11ali ty o f eggs may
also suffer. In this photograph the
light is being ref1ected from the outer
rim of a watery egg white ancltherc is
no intcmal ring of albumen.

43
 113
Egg drop syndrome '76
(127 adenovirus/BC14 infection)

113 This infection is characterised by a drop in egg production

or by a failure to peak in laying fow l. Both may be accompanied
by the production ofabnormally shelled eggs. These specimens
are ridged, irregularly shaped and some have very thin shells.
Soft-shelled and shell-less eggs may be seen.

Infectious avian encephalomyelitis

(epidemic tremor)

114 Terminal stages as in this 14-day-old chick may be

preceded by ataxia. Muscular tremors may also be appreciated.
Diagnosis is supported by histological examination of brain,
spinal cord , pancreas , proventriculus, gizzard and heart. The
disease occasionally occurs in turkeys.

115
115 A non-purulent encephalomy-
elitis is widely distributed throughout
the spinal cord and brain. Degenerate
neurons often exhibit central chroma-
tolysis (arrows). This is not a patho-
gnomonic feature but it can be a useful
diagnostic sign as more neurons show
degeneration of this type than in, say,
either Marek's d isease or Newcastle
disease.

44
 116
116 A brain stem neuron undergoing
central chroma10lysis. The nucleus
has moved to the margin of the cell.
Note the surrounding gliosis.

,
y-

117
117 Visceral lesions are characte-
rised by the presence of lymphoid
infiltration. The pancreas normally
contains a few lymphoid foci but in
this section there is an increase in their
number.

118 Higher power examination of

one of the foci from 117 shows that it
is mainly composed of immature
cells.

45
119 Lymphoid infihration in the
proventJiculus is restricted to the
muscularis. Similar infiltration may
m:cur in the muscle of the gizzard and
myocardium.

Viral arthritis and tenosynovitis

120
120 Ruptured gastrocnemius tendon
as a result of chronic tendinitis in a
broiler. Experimental reovitus infec-
tion (see 292).

121 Ruptured digital flexor tendons

in a broiler. Reovirus was isolated
from this fleld case.

46
122 123

122 Tenosynovitis in a broiler. The tendon sheath is thickened 123 Arthritic lesion with pitting of
as a result of a non-purulent inflammation involving a heavy the articular cartilage over the distal
infiltration of lymphocytes and plasma cells. Experimental tibiotarsal condyles in a broiler.
reovin1s infection. Experimental reovirus infection .
(see 30).

Marek's disease (including transient paralysis)

124
124 Paresis of the right leg. If both legs are involved a
characteristic posture is often taken up with one leg pointing
forwards and the other held backwards under the body.

-
125 This normal sciatic nerve demonstrates the presence of
cross striations. These arc best seen in daylight rather than
under artificial light and are gradually lost as post-mortem
changes advance. In \!1arek ·s disease. if neural lesions are
present. the first appreciable change is a loss of the normal
striations together with some focal swelling and yellowing.

47
126 One brachial plexus is grossly
enlarged. It is important to compare
the vagal. brachial. intercostal.
mesenteric and sciatic nerves both in
the same bird and between indi -
viduals within a batch . otherwise
slight swelling which may evenly
affect most of the peripheral nerves
can be missed. There is little doubt
about the diagnosis of Marek's dis-
ease when gross neural lesions arc
found. Doubt arises when tumours
arc present in the organs in the ab-
sence of peripheral nerve enlarge-
ment. It is then necessary to examine
both the nerves and neoplastic ti ssue
histologically.

127
127 Small lymphocytes are aggre-
gated around an intraneural capillary
(type C lesion). A few plasma cells
are often present in lesions of this
type.

128 An infiltration of small lympho-

cytes and plasma cells in a peripheral
nerve is accompanied by oedema
(type B lesion).

48
 129
129 The tumorous spleen has rup-
tured and the subsequent haemor-
rhage caused the death of th is 6-week-
old broiler.

130 Tumour of wing muscle.

Muscular and provcntricular tumours
occur more frequently in ~arek · s dis-
ea. e than in lymphoid leukosis.

13 1
131 Grossly enlarged li\'er. Marek· s
disease tumours may involve most of
the abdominal and thoracic viscera
although the distribution varies con-
siderably.

49
 132
132 Skin tumours are uncommon in
Britain but are sometimes encoun-
tered in broilers at slaughter. Most of
the tumour formation in this specimen
is taking place around the feather
foll icles.

133
133 This small intestinal vil lus con-
tains a !aminal infiltrate of neoplastic
lymphoidcells . The epithelium on the
right is also parasitised with coccidial
fom1s which arc similar to those of
Eimeria acervulina. Concurrent in-
fection with coccidia is often
observed in affected birds on deep
litter.

134 The population of neoplastic

cells in Marek's disease tumours is
nearly always pleomorphic. The sec-
tion of skeletal muscle demonstrates
this feature . A large dark staining cell
is visible centrally. this is a so-c'alled
Marek's disease cell and is probably a
degenerative lymphoblast. These
cells are useful diagnostically but are
relatively infrequent. NB The type A
lesion of peripheral nerve is also com-
posed of proliferating mixed lym-
phoid cells.

50
135 The cut surface of lhis liver de-
monstrates grey areas of lymphoid
infi Itration round the portal triads and
central veins. This type of infiltration
is frequently seen in Marek's disease.

136 This section of an au tolysing

vi~ceral tumour demonstrates numer-
ou~ pyknotic nucki within degenerat-
ing neoplastic lymphoid cells. Pyk-
nosis tends to be seen more frequentl y
in au tolysing lesions of Mare k's dis-
case than in those of lymphoid leuko-
~is (see J.t6).

137
:: ·. . .. :. .:~ -~ (;.;~
137 Dense perivascular cuffing is a ' ,.,; ..·...
feature of an encephalitis which
affect~ some birds.

~--

.•
~
" ..~....
.. .:
' r

51
 138
138 Transient paralysis. This pullet
shows t1accid paralysis of the neck
and tail.

139 A perivascular cuff in the brain

of a bird showing signs of transient
paralysis . Note the small cyst-like
foci of nuclear debris (arrows) .

Lymphoid leukosis and other tumours caused by the

leukosis/sarcoma group of viruses
140
140 The liver of thi:; adult fowl is
greatly enlarged due to cxtensi ve neo-
plastic infiltration. In the past this
condition was often called 'big liver
disease'. Although hepatic tumours
are often found, the macroscopic
appearance of the liver cannot be re-
lied on for diagnosis.

52
141 Lymphoid tumours affecting the
kidneys and bursa of Fabricius in the
same bird depicted in 140.

142
142 Tumour formation causing great
enlargement of the bursa of Fabricius
and f~cal hepatic lesions in an adult
fowl.

143
143 Tumours arc focal and grow by - ..,.-..·~.r:iin'<C
expansion. This contrasts w ith the
more infiltrative lesions of Marek· s
disease. Cords of hepatocytcs are
being compressed between expand-
ing foci in this liver.

53
144 Expansion of the primary intra-
follicular tumours taking place in the
bursa of Fabricius.

145 Tumours are composed ofsheets

of immature cells which show little or
no pleomorphism. frequently . the
nuclei are surrounded by a clearly
defined rim of cytoplasm and contain
large violet-staining nucleoli.

146 Many of the tumour cell nuclei

undergo karyorrhexis during auto-
lysis (see 136).

54
 147
147 Myeloid leukosis. Chalky white
myelocytomas are present on the ster-
num and ribs of this fowl .

148 Myeloid leukosis. Lm·ge mnn-

bers of proliferating myeloc.ytes in-
filtrating skeletal muscle.

149 Erythroid leukosis . The liver of

this fowl is greatly enlarged and
cherry red . Similar lesions may occur
in the spleen. The condition is rare.

55
 ISO
ISO Osteopetrosis. Cross section of
an affected tarsometatarsus in a fowl
shows the great increase in thickness
of the cortical bone.

151
151 Nephroblastoma. This may be
encountered in some fowl as a large
tumour that has replaced a division of
the kidney. They may be cystic. His-
tologically they are very variable. ln
this section tubular structures are sur-
rounded by masses of undifferenti-
ated cells.

152
152 Nephroblastoma. Keratinised
fonns of nephroblastoma are seen
from time to time. Large whorls of
keratin in this lesion are surrounded
by a rim of epithelial cells.

56
Lymphoproliferative disease of turkeys
154
153

153 Greatly enlarged liver in a IS-

week-old grower. This bird also had a
Pseudomonas aeruginosa septi-
caemia. The spleen is often very en-
larged in this condition.

154 Diffuse tumour of heart.

155 Section of liver showing the

pleomorphic nature of the lymphoid
tumour.

156 The lesion in ISS seen at higher

magnification.

156

57
Reticuloendotheliosis virus induced tumours in turkeys
157
157 Experimental infection. The le-
s ions are focal and grow by expan-
sion. This section demonstrates the
population of primitive lympho-
blasts.

58
 Other neoplasias

Adenocarcinoma of the reproductive tract of the hen

158 Carcinomas may arise from
either the ovary or the oviduct. In this
specimen the oviduct is principally
involved hut primary ovarian lesions
arc also common. The tumour tissue
is pale and very firm on palpation.
Lesions are seen towards the end of
lay as a sporadic cause of death but
occasional outhrt;aks occur.

159 These tumours usually mctasta-

sise to serous surfaces in the abdomin-
al cavity and particularly affect the
pancreas. intt;Stine and its mesentery.
The metastatic nodules on the vi cera
are frequently rounded.

160 Most of the metastases are scir-

rhous in nature due to the proliferation
of connective tissue in response to the
invading carcinomatous cells.

59
Leiomyoma of
the oviduct ligaments
161 These tumours (arrow) are often
found in the ventral ligament and are
usually composed of both smooth
muscle and fibrous elements.

Squamous cell
carcinoma of the skin
162 Multiple small crater-like le-
sions are occasionally found on in-
spection of broiler carcases at slaugh-
ter. Individual ulcers may coalesce.
patticularly on the back.

163 A keratin 'pearl' surrounded by

squamous cells. The tumours invade
the dermis and subcutaneous tissue
but do not seem to metastasise during
the commercial life of the broiler.

60
 Fungal diseases
Aspergillosis
164
164 Miliary lesions of pneumonia
caused by A .fumigaws in a 7 -day-old
chick that had been infected from
contaminated straw Iiller. If infection
is acquired in the hatchery - a rare
event these day - pneumonia can
develop by2daysofage. Occasional-
ly, lesions are confined to the bronchi
and are not seen unless the lung is cut
through .

165 The miliary lesions in the lungs

consist of rapidly developing granu-
lomas. PAS-hacmatoxylin.

166
166 Necrotic tissue is quickly re-
moved by g iant cell activity. In this
section hyphae are protruding
through a ring of giant cells PAS-
haematoxylin.

61
167 Infections in chicks and turkey
poults often result in the development
of small nodules on the surface of the
thoracic and abdominal air sacs.
These lesions have a concentric
appearance an.d a depressed centre.
Later growing stages in the turkey
may be affected by an air sacculitis in
which there arc much larger plaques
of pus present.

168
168 Heavy pulmonary infections in
young birds may lead to focal en-
cephalitis. Small hyphae in the brain
stem of a turkey poult arc surrounded
by an intense inflammatory reaction
and some attempt at early giant cell
formation. PAS-haematoxylin .

169
169 Conidiophores are sometimes
seen if pulmonary lesions extend into
an air space.

62
 170
Dactylariosis

170 Occasional outbreaks may result

in severe losses in both chicks and
poults. Dactylaria gallopava. intro-
duced as a contaminant on bark litter,
caused heavy mon ality in broilers on
the fam1 from which this specimen
was obtained . Pulmonary lesions
were minimal but severe cerebellar
and brain stem lesions caused an out-
break of disease which clinically re-
sembled encephalomalacia. The in-
fection has destroyed most of the
posterior fol ia. PAS-haematoxylin.
171
171 Higher magnification of 170
shows slender hyphi!f'. ensheathed by
newly formed giant cells. PAS- •
haematoxylin.

172
172 Young colonies of D. xallopam
growing on Sabouraud's medi um
after 48 hours growth at 42°C.

63
 173
Candidiasis
173 A heavy deposit of desquamated
epithelial cells provides the typical
' turkish towelling ' appearance. Can-
dida albicans infection.

174
174 Most of the fungal growth takes
place in the mass of degenerate
"fluames hut some invasion of the
intact epithelium usually occurs. The
pseudohyphae are poorly demon-
strated with haematoxylin and eosin
but arc strongly positive to PAS
and other fungal stains. PAS-
haematoxylin.

175
175 Pseudo-hyphae within crop
epithelium. PAS-haematoxylin .

64
 Parasitic diseases
176
Ascaridiasis
176 Heavy infestations with Ascar-
idia galli are not common under inten-
sive systems of husbandry. Intercur-
rent disease such as Marek's disease
may be present.

Capillariasis
177
177 lnfesrmion ofrhe small imesrine
may have a marked effect on egg
production in fowls maintained on
deep liner. The affected bowel is
usually pale and distended with lluid
contents; the mucosa is slightly
roughened. The worms are difficult to
see with the naked eye but are easily
visible in smears. This photograph
demonstrates the hi-operculate eggs
within a female worm.

Coccidiosis 178
178 f 'imeria tenet/a. Caeca of a
yo ung pullet distended with blood.

65
179 E. tenel/a. Extreme pallor of the
pectoral muscles as a result of caecal
haemorrhage.

180 E. tend/a. Caeca opened to 180~~----------~----~---------,

show haemorrhagic debris. There
may be firm caecal cores in subacute
cases or in birds that are recovering .
These cores are not usually adherent
to the mucous membrane.

181 E. tenella. Smears of the

haemorrhagic mucosa will demons-
trate the large second stage schizonts.
T hese arc best viewed under a fairly
low illumination of the microscope
stage .

66
 182
182 E. tenella. Second stage schi-
zonts (containing merozoites) in dis-
rupted caecal mucosa.

183
183 Eimeria necatrix. Distended
small intestine showing mocrled
haemorrhages through the serous
surface.

184 E. necatrix. Opened intestine

from 183. The lum.e n is full of mucoid
debris. Haemorrhage is usually more
pronounced. Mucosal smears show
similar second stage schizonts to
those observed in £ . renel!a
infestations.

67
185 E. necatrix. Oocysts are found in the
caecum and, in this photograph, are dis-
185

.... .....
~ . _ $
.. , ...
t .
tending a crypt. t •
.'
•

186
186 Eimeria mCLrima. Small intestinal
mucus is often orangey-brown in colour.

187 Eimeria acervulina. The mucosal

surface of this intestine is roughened and
slightly congested. The affected broiler
breeder had concurrent lesions of
Marek's disease. Small transverse white
flecks can often be detected on the serous
surface of the parasitised intestine.

68
188 £. acervulina. Dense parasitisa-
tion of the small intestinal epithelium.

189 f::imeria bnmerri. The lesions

usually affect the lower part of the
small intestine and the colo- rectum
but can be more evenly distributed
throughout the small intestine. This
species causes se,·ere necrosis of the
superficial mucosa. which i difficult
to distinguish grossly from uncompli-
cated cases of necrotic enteritis (see
37 ). Secondary bacterial hepatitis
may occur in birds that surYive for
more than a few days.

190 F.imeria meleaf?rimitis . The

small intestine of this turkey poult is
distended with pale fluid contents.

69
 191
Histomoniasis (Histomonas meleagridis)
191 The disease is now a rarity in turkeys except in small flocks
that have access to ground used by chickens. The caeca are
distended with cores of inflammatot)' debris that are firmly
adherent to the mucous surface. Localised pe1itonitis is often
present. The focal liver lesions are rounded and have paie rings
sun·ounding a darker central area. The condition occurs occa-
sionally in the fowl.

192
192 A section of an infected caecum
shows the small rounded forms of the
parasite. The histomonads may be
more difficult to identify histological- ..
ly in resolving lesions in the liver but
should be readily seen during the
acute stages. PAS-haematoxylin.

193
Cryptosporidiosis
193 The small basophilically staining para-
sites are present on the surface of the luminal
epithelium in the bursaofFabricius in a broiler.
The epithelium is hyperplastic . Similar lesions
may be observed in the trachea. No ciinical
signs were shown in this case but respiratory
disease has been reported both in turkeys and in ·
broilers. The small size of these organisms
makes them difficult to see. They stain strongly
with PAS .

70
 194
Scaly leg
194 The presence of the parasite
Knenzidocopres mutans has caused the
leg scales of a bantam to become
raised due to the accumulation of de-
bris undemeath.

195
Lice
195 Large numbers of eggs (species
unidentified) on feathers of a laying
fowl from a flock where egg produc-
tion was poor.

Red mite (Dermanyssus

gallinae)

196 These parasites feed mainly at

night and are usually found off the
host. Their presence should be sus-
pected in layers if egg production falls
and anaemic birds are submitted for
examination. Note the red colour of
those m ites that have recently fed .
The mites are shown at about ten
times life size.

71
Northern fowl mite (Ornithonyssus svlviarum)

197 These mites live continuously

upon the birds. They are seen here on
the feathers of a broiler breeder that
was submitted with excoriated tail
and vent skin. These mites move
quickly and are easily transferred to
the gloves and anns of the person
doing the post-mortem examination.

72
 Nutritional deficiencies and
metabolic disorders
Riboflavin deficiency
199

200
198 Clubbed down may occur in the
unhatched embryos and day old
chicks from parent flocks that receive
inadequate levels of this vitamin. .

199 Curled toe paralysis. Young

chicks may show clinical signs at
aproximately 10-14 days of age if
they have been eating a deficient
ration. The birds remain alert hut are
unable to rise from their hocks. They
exhibit a flaccid paralysis and in-
curling of the toes, which is not main-
tained after death .

200 The sciatic nerves are swollen

and, on a white background, look
discoloured.

201 Section of a sciatic nerve from a

broiler chick with curled toe paralysis
shows Schwann cell proliferation.

73
Encephalomalacia (crazy chick disease)
202 203
r-------------------------------------------------~

204
202 Opisthotonos in a 5-week-old
pullet replacement. Clinical signs arc
most often seen between 2 and 3
weeks of age if chicks or turkey poults
have been on a ration that is either
deficient in vitamin E or one from
which they are unable to obtain a
sufficient amount of the dtamin.

203 Haemorrhage within a partly

fixed cerebellum of a 2-week-old tur-
key poult. When present, gross le-
sions vary from extensive haemor-
rhage of the cerebellum to a barely
detectable oedema and ilanening of
the cerebellar gyri and of the cerebral
hemispheres.

204 Cerebellar haemorrhages.

Haemorrhage usually occurs in
severe lesions but it is not always
present.

205 Focal malacic lesion in a cere-

bellar medullary ray. The malacia
may be extensive or restricted to small
punctate lesions. the latter being seen
particularly in younger chicks. The
lesions arc most frequently observed
in the cerebellum and brain stem but
can also affect other parts of the brain.

74
 206
206 Hyaline capillary thrombi are
often associated with the malacic
foci. Martiu~ ~carlet blue.

Rickets
207 Rickety rosary in a 3-week-old
chick . Field outbreaks appear to
occur more frequently in turkey
poults. The condition is usually
caused by a deficiency of vitamin D
but may also be produced by a lack of
calcium or phosphorus or by an imba-
lance of these two minerals. An in-
ability to rise from the hocks and
severe depression are the principal
clinical signs.

208 Beading of the rib heads is a

common feature.

75
209 210

211
209 Post-mortem assessment of
bone strength may be difficult in any
bird under 2 weeks of age but in
rickets the tarsometatarsi are usually
rubbery and do not break cleanly
under pressure. Displacing the beak
also provides a good indication of the
strength of the facial bones.

210 The growth plate cartilages of

the long bones arc often thickened and
poorly penetrated by blood vessels.

211 The columns of cartilage cells in

the .growth plate may be irregularly
aligned. 3-\veek-old pheasant PAS-
Aician blue .

212 The parathyroid glands are

sometimes markedly enlarged. This 212
section shows a cord-like arrange-
ment of parenchymal cells and prolif-
eration of stromal connective tissue
from a severe case in a 3-week-old
broiler. Acryl ic resi n , Lee's
methylene blue-basic fuschin.

76
Calcium deficiency in adult laying fowl
213 Twisted sternum. The sternum
and rib cage are frequently soft and
distorted. Egg production drops and
the shells are thin.

21~
214 Sigmoid Ocxure of the ventral
part (arrows) of two ribs caused by
patholog ical fractures.

215 Fractured rib seen in 214. One

cortex is s hown.

77
Fatty liver and kidney syndrome
216
216 The condition has been tradi-
tionally associated with broilers but
has also been known to cause mortal-
ity in commercial layer chicks. Such
chicks are seen here with ruft1ed
feathers, depression and some are un-
able to rise from their hocks. Out-
breaks of the condition have been
largely prevented by the inclusion of
additional biotin in rations.

217 The subcutaneous fat is con-

gested. This feature gave rise to the
name 'pink disease' .

217 218

219
218 Livers are pale, often in a rather
streaky fashion, and friable. It may be
difficult to cut blocks of this tissue for
fixation.

219 Subcapsular haemorrhages may

be present at necropsy. Although it is
not demonstrated in this specimen ,.
such haemorrhages are usually clus-
tered near the posterior tips of the
lobes (see 90) .

78
220 Most kidneys contain pale areas
of tissue which contrast with the deep
reddish brown colour of the nonnal
organ. The kidney of this broiler was
severely affected and had an even
pallor. Note the outline of individual
lobules within the renal divisions.

221
221 A pale heart (left) from an
affc::<.:ted broiler contrasts with the
nonnal colour of the organ in an older
bird.

222
222 The small intestinal contents .
especially those of the duodenum.
may be very dark and possess a strong
odour.

79
223 A large quantity of fine lipid
droplets are contained within the pro-
ximal convoluted tubular cells of this
kidney. Oil red 0. Histological con-
firmation of this disease requires de-
monstration of lipid in the kidney,
liver and heart.

224 Fat droplets within the myocar-

dium of a broiler. Oil red 0.

80
 Diseases of uncertain
or unknown aetiology
Fatty liver haemorrhagic syndrome in laying fowl
225 A large blood clot surrounds the
ruptured right lobe of the liver in a
obese layer. Note haemorrhages in
the unmptured left lobe. The bird may
survive several haemorrhagie epi-
sodes, particularly if escaping blood
is confined within the lobes or as a
subcapsular haematoma. The condi-
tion occurs in obese birds; both meta-
bolic and environmental associations
have been implicated.

226 A large abdominal blood clot

arising from the ruptured liver of an
adult commercial layer. Note the pale
comb in the decapitated head of the
same bird.

227
227 Cut surface of one liver lobe .
The block was taken in an area where
haemorrhage had not occurred. The
tissue is usually extremely friable and
it can be difficu lt to obtain suitable
blocks for histology. It is usually bet-
ter to put large po11ions into fixative
and trim after 24 hours.

81
 228
228 Excess fat in the ruptured liver of
an obese layer. Sudan IV.

229
229 LJeath may occur in obese layers
without haemorrhage taking place.
Fine droplets of lipid are exuding
through the liver capsule. Note the
pad of abdominal fat.

230
230 The presence of reticulin is de-
monstrated in the blood vessel walls
but not in the surrounding parenchy-
ma. The lesion has been described as a
reticulolysis. Gordon and Sweet.

82
231 Reticulin network in nom1al
liver demonstrated by the same
technique as in 230.

232 This syndrome may cause death

in broiler flocks from the end of the
first week onwards. Males are more
frequently affected than females.
Most carcascs are found on their
backs. Note the good condition of this
carcase and the lack of any muscular
congestion.

233
233 Bilateral pulmonary congestion
and oedema is the principal finding at
necropsy. The digestive tract i!S full of
food and there may be some pallor of
the intestine. liver and kidneys.

83
 234
234 Pools of serosanguinous fluid
often remain between the ribs after the
lungs have been removed.

235
235 A section of lung confirms the
intense congestion seen post mortem.
The airways are full of proteinaceous
fluid (arrows). There may be haemor-
rhages in the mucosa of the secondary
bronchi.

Sudden death syndrome in laying fowl

236
236 A common cause of sporadic
death in both commercial and breed-
ing birds that are in full lay. Protru-
sion of congested cloacal tissue
through the vent is the only external
feature.

84
 237
237 Intense congestion of the blood
vessels on the surfact: of the ova and
variable pulmonary congestion are
frequently seen as post-mortem fea-
tures. A broken, shelled egg is some-
times found in the shell gland.

Cardiohepatic syndrome in turkey poults (' hepatosis ')

238
238 Typically. the syndrome occurs
at 7-I 0 days of age but may be seen up
to 3 weeks of age . Poults are not
usually seen ill and arc found dead.
Dilation of the right side of the heart .
ascites. a pale slightly "brittle· liver
and generalised venous congestion
are the main post-mortem features.
The relationship of this condition to
the appearance of similar gross le-
sions in older turkeys is uncet1ain.

239 L iver sections reveal non-fatty

vacuolation of hepatocytes and the
presence of round PAS-positive cyto-
plasmic bodies. PAS-hacmatoxylin.

85
 240
240 The rounded cytoplasm ic bodies
within degenerating hepatocytes also
staineosinophilically. One such body
(arrow) is seen near the centre of this
photograph.

Ascites and congestive heart failure in broilers

241
241 A common condition mainly
occurring in male broilers. Frequent-
ly seen as an incidental finding in
many nocks but there may be occa-
sional outbreaks. There is severe
ascites and a marked passive venous
congestion throughout the carcase.
. ote the deep red colour of the mus-
culature.

242 The ascitic t1uid may be semi-

clotted. The liver is small and has
rounded borders. Dilation of the right
side of the heart and intense passive
congestion of the lungs and other vis-
cera are the main findings . The ter-
minal stages are analogous to conges-
tive heart failure.

86
243 Comparison of an affected liver
(left) with a normal organ.

244
244 I ,ow power view of a chronic
liver lesion. A fibrinous deposit on the
surface of the liver is partly organ-
ised. Other features not seen in this
photograph include dilation of the
intrahepatic branches of the hepatic
vein and a variable increase in paren-
chymal connective tissue. Martius
scarlet blue.

245
245 Dead birds are also found in
affected Bocks with hepatic lesions
that may represent an earlier stage of
the condition . Grossly, such livers are
swollen, discoloured and often have a
mottled or dimpled surface. In this
specimen dimpling is not present but a
fine reticular pattern of pale bands of
tissue can be seen through the
capsule.
246 Sections from a liver such as that
in 245 reveal, initially. a marked
hepatocytic fatty change that mainly
affects periacinar tissue. This is
quickly succeeded by coagulative
necrosis of the affected zones. Here. a
central band of surviving hepatocytes
is t1anked by degenerating cells on
either side. vacuolation (fatty) is
apparent at the junctions (arrows) of
the viable and degenerating hepato-
cytes. Haemorrhagic replacement
and heterophi lic infiltration arc vari-
able features of such lesions.

Round heart disease

247 This condition is now uncom-
mon but at one time was seen as a
cause of sudden death during winter
months in fowls maintained on deep
litter. The enlarged heart usually has a
blunted apex in which there may be a
central depression.

248 Degenerative fatty changes in

swollen heart muscle fibres cut in
cross section. Note also nuclear de-
generation.

88
DyschondropIasia
249 Seen in both broilers and turkey growers.
It is more common in male birds. This cartilage
abnonnal ity may be present at the ends of all the
long bones in the leg and has been reported in
the humerus. The tibiotarsus is most frequently
affected and in this 6-week-old broiler the
upper part of the bone is severely defonned.

250
250 The top bone is a tibiotarsus re-
moved from the broiler in 249. It has
been split to show the large posterior-
ly bent head containing a plug of
abnonnal cartilage (arrows). Patho-
logical fractures arc present on both
the anterior and posterior aspects.
The bone below is nom1al.

25 1
251 The head of this tibiotarsus is
also bent posteriorly. A large mass of
abnormal cartilage extends from the
growth plate into the metaphysis.

89
252 253

252 The lesion has been panially re-

solved in this bone but a substantial
quantity of abnormal canilage still
remains.

253 Varus defom1ity of tarsometa-

tarsi associated with large medial
plugs of canilage in a broiler of
slaughter age. Many broilers are
affected by dyschondroplasia but do
not have defonned legs unless the
lesions are large.

254 Low power view of a shallow

dyschondroplastic lesion in the
proximal tarsometatarsus of a broiler.
Martius scarlet blue.

255 An area of abnom1al cartilage in

the metaphysis. The metaphyseal
blood vessels are numerous but. those 255
near the periphery of the hypertrophic
canilage appear empty (arrows) and
hardly invade the cartilage. Martius
scarlet blue.

90
256 The lack of blood supply to the
hypertrophic cartilage leads to necro-
sis of the distal cells. Necrotic cartil-
age cells containing eosinophilically
staining nuclei are scattered amongst
other surviving cells .

Valgus leg deformity in broilers ('twisted leg')

257
257 Valgus deformity is seen from
two weeks of age onwards and may
affect either one or both legs . Males
are more often affected than females.
Affected legs bend outwards at the
hock joint. Posterior aspect.

258
258 Removal of the musculature
shows that in most cases the deformi-
ty results from a lateral tilting (rather
than twisting) of the distal tibiotarsal
condyles. Amerior aspect.

9!
 259
259 Progressively severe defonnity
affecting three legs from left to right.
As the condition becomes more se-
vere the gastrocnemius tendon slips
off the joint and usually comes to lie
laterally over the bone. Anterior
aspect.

260
260 The lateral deviation of the distal
tibiotarsal condyles . may be suf-
ficiently severe for them to become
separated from the shaft of the bone.
In this broiler the shaft has come to lie
underneath the skin just above the
hock joint.

261 A dissected hock joint of a broil-

er shows the condyles at right angles
to the shaft of the bone. Dyschondro-
plasia may be found in the distal
tibiotarsus of some severely de-
formed cases .
 262
Twisted leg
in turkeys
262 The lower third of the bottom
tibiotarsus has rotated laterally. This
process produces a similar overall
effect to valgus deformity of the legs
in broilers ("twisted leg') . but is usual-
ly restricted to one leg and is a true
rotation of the shaft. It is occasionally
seen in broilers.

Renal failure (visceral gout)

Renal failure is a common cause of death in fowls of uncertain. Visceral gout, ie the deposition of urates on
different types and ages . It is also seen in the turkey. the surfaces of the viscera and in the joints. should not be
Apart from recognised causes of renal disease such as regarded as a single entity but as an end stage of possibly
neplu·itis induced hy infectious bronch itis virus, water many di ffcrent renal diseases. Generally, kidney disease
deprivation. and excessive intake of protein and calcium is more prevalent in adult laying fowl.
the aetiology of many of the nephritides and nephroses is

263
263 Baby chick nephropathy may
occur during the first week of life and
cause heavy mortality. Birds may die
shortly after hatching. The kidneys
arc swollen and urates are usually
deposited on the viscera and in the
joints (visceral gout) . Histologically.
there may be scal!ered foci of necrotic
tissue throughout the cortex or dila-
tion and inOammation of the collect-
ing duct system and ureteral
branches.

93
 264
264 Urolithiasis. This condition has
become more prevalent in laying
fowl. Affected birds usually remain '
in lay until shortly before death. The
carcases are congested. One or both
kidneys show signs of atrophy. The
ureters are greatly distended with
mucus and uroliths.

265 Urolithiasis. This adult broiler

breeder hen died in good bodily con-
dition. One kidney has almost com-
pletely atrophied. Compensatory
hypertrophy has taken place in the -
divisions of the opposite organ which
is drained by a large distended ureter
(arrows). Urates are present on the
surface of the epicardium.

266 Urolithiasis. A greatly dis-

tended ureter on the left almost
obscured the atrophic kidney on that
side. Compensatory hypertrophy has
taken place on the right. These kid-
neys were dissected from an adult
commercial layer.

94
267 Urolithiasis. Dilated collecting tubules in a
medullary tract of an adult laying fowl. Masses of
inflammatory cells are present within the tubules.
There is usually an interstitial nephritis.

268 Urolithiasis. A focal area of necrosis within

the cortex, probably resulting from coalescing
degenerate proximal convoluted tubules. Note
dilation of the surrounding tubules and flattening
of their epithelium.

269 The cross-section of the kidney on the right

emphasis the considerable size that hypertrophied
renal divisions may anain. The tissue on the left of
the photograph, although fairly autolyscd, de-
monstrates the size of the corresponding division
in a normal kidney obtained from a bird of similar
age.

270 Visceral gout. Deposition of

urates on the epicardium.
269

95
r

271 Visceral gout. Urates contained

within a hock joint.

272
272 Visceral gout. Urates present on
the surface of the liver, abdominal fat
and sternum.

273
273 Articular gout. Periarticular de-
position of urates in two feet. Normal
foot on the right for comparison.

96
 274
274 Visceral gout. Tophus formation may
occur terminally in the kidney and other tissues
such as the liver and spleen. In this renal focus
the urates have dissolved out of the tissue
during processing but the radial pattern of their
deposition is still visible.

275
275 Visceral gout. Tophus fom1a-
tiun within lht:: \.:orlt::x ( lissut:: fixt::d in
absolute alcohol and stained by
the Gomori methenamine silver
method).

Stunting syndrome of broilers (malabsorption)

276
276 This is a transmissible condition
which becomes most noticeable clini-
cally during the second week of life.
Both of the birds shown are 23 days of
age. Note the retention of chick down
on the small bird and also the abdo-
minal protrusion. Abnormalities of
the primary wing feathers may result
in a "helicopter" appearance.
277 Gross lesions vary in different
ombreaks. One of the features of the
disease in Britain has been the appear-
ance of pancreatic lesions . A pale
fibrosed pancreas (bottom) in a
stunted 5-week-old broiler is com-
pared with the normal gland in a 3-
week-old specimen from the same
fann. Pancreatic tissue at the closed
end of the duodenal loop is usually
affected first.

27R The lesions are mllinly confined

to the exocrine pancreas. Early stages
of degeneration, atrophy and fibrosis
are taking place. There is consider-
able vacuolation of the acinar cells
and only a few of these contain
zymogen granules. Acrylic resin.

279 High power view of the abnor-

mal pancreas . The ac inar cells on the
right contain 2ymogcn granules but .
these are absent in the tissue on the
left. Acrylic resin. haematoxylin
ponceau fuschin.

98
 280
280 Side view of the distended abdo-
men in a 2-week-old broiler.

.• .
~~
281
281 The intestines are pale and di-
lated. this di lation giving rise to the
abdominal distension. Undigested
food is present in the lower bowel.
The pale pancreas (arrow) can be seen
in the duodenal loop.

282
282 Proventricular swelling has
hccn a less common find ing in Bri-
tain.

99
283

283 Atrophy of thymus in a 3-week-

old broiler. The vagal nerve is lying
dorsally to small reddened portions of
gland.

284 Rickety changes may affect the

skeleton. Note swollen rib heads from
a stunted broiler on the left compared
to a normal specimen (see208 ).

Acute pectoral myopathy of broiler breeders

285
285 A sporadically occurring con-
dition in immature birds during the
rearing period. Affected birds are not
usually seen ill. Gelatinous fluid is
often present in the subcutaneous tis-
sue overlying the breast and also sepa-
rates muscle fibre groups within the
Musculus pectoralis. Pools of this
fluid may collect between theM. pec-
toralis and theM. supracoracoideus.

100
 286
286 Severe myodegeneration in aM.
pectoralis. Masson's trichrome.

287 Contraction of necrotic seg-

ments of cytoplasm in three fibres of
theM. pecmralis. Note the pale blue
staining nuid filling the emptied por-
tions of the cmlomysial tubes. Mas-
son· s trichrome.

101
 Miscellaneous conditions
Spondylolisthesis
(kinky back)
288 Clinical cases are usually seen in broilers between 3 and 6
weeks of age. Birds squat back on their hocks and cannot stand .
One or both feet are often slightly raised from the surface on
which they arc placed.

289
289 The condition is caused by a
downward rotation of the sixth thor-
acic vertebral body. If sufficiently
severe, this results in a failure of the
interarticular facets between the sixth
and seventh thoracic vertebrae with
the result that the sixth vertebra
moves ventrally and compresses the
spinal cord (arrow).

290
290 Spinal cord w ith compressed
zone (arrow) .

291
291 Section of spinal column at T6/
TI showing compression of spinal
cord.

102
 292
Ruptured gastrocnemius tendon
292 This may occur sporadically. usually in heavy fowl such as
capons and broiler breeders. but is occasionally seen as an outbreak.
The condition may be uni- or bilateral. Viral arthritis should be
suspected if the rupture has heen preceded by a chronic tendinitis
and tenosynovitis (see 120-1 23).

Deep pectoral myopathy

293
293 Occurs in turkeys and broiler
breeders. The condition is usually
observed at meat inspection. The le-
sion may affect either one or both of
the deep pectoral muscles (M. supra-
coracoideus). This turkey breeder
carcase has dished pectoral muscula-
ture on the right of the photograph. A
black line has been drawn over the
breast to d istinguish the two sides.

29~
294 TheM . supracoracoideus is con-
tained in an osteofascial compa!1-
ment. Abnonnal exercise for birds of
this type such as undue napping of
wings may in some individuals lead to
swelling of the muscle and occlusion
of its blood supply. ccrosis results.
The fascia of the muscle of this 33-
week-old broiler breeder has been cut
anteriorly to show the bulging
affected tissue (arrows) of the acute
lesion. The early lesion is accompa-
nied by the production of gelatinous
fluid.

103

- - - ·- - -
 295
295 The bottom muscle is an affected
M. supracoracoideus that is under-
going atrophy. The necrotic tissue is
often an unusual apple green colour.
The medio-ventral aspect is shown .

296
296 Cross sect ion of affected and
unaffected M . supracoracoideus. The
necrotic tissue·is crumbly and dry.

297 Cooked lesion. The green colour

is retained.

104
 298
298 Fragments ofnecroticM. supra-
coracoideus (arrows) adhering to the
sternum of a turkey breeder.

299
299 Junctions of normal and affected
M. supracorac ohleus. The necrotic
tissue below is s taining more palely
with eosin than the viable muscle
abO\'C.

300
300 Muscle fibres with in an affec ted
M. supracoracoideus. These exhibit
discoid necrosis.

105
Plantar pododermatitis
301
301 The plantar surface of the foot-
pads of heavy broiler breeders and
turkeys may become severely ulcer-
ated and caked with litter. This is seen
most freq uently when the litter condi-
tions are poor , particularly if flocks
are scouring.

Moult
302 Although obviously not a dis-
ease, moult may be precipitated by
eventS such as accidental water de-
privation. A large number of new
feathers arc growing on the back of
this broiler breeder.

303 The ovaries of birds that are pro-

ducing new feathers are inactive.

106
304 Moult must be distinguished
from feather loss on the back as a
result of mating activity in breeding
f1ocks. Short stubby ends of broken
feathers arc usually apparent in these
birds.

Persistent right oviduct

305 CystiC dilation of this stmcture
(indicated by blue pointer) is a fairly
common post-mortem finding . In
some cases the cystic remnant may
become very large and compress the
abdominal viscera. Death can result.

Internal layer
306
306 Three large soft shelled eggs
were found in the abdomen of this
commercial layer. The magnum was
constricted at one point and had not
pem1itted normal passage of eggs
through the oviduct. Several more
eggs arc retained within the duct.
Either soft or hard shelled eggs are
occasionally found within the abdo-
minal cavity of laying fowl that
possess patent oviducts. These may
be adherent to the peritoneum.

107
 307
Prolapse of oviduct
307 The lower part of the oviduct is
protruding through the vent.

308
Cannibalism
308 In laying fowl the vent is most
frequently attacked . At post-mortem
examination most carcasses are pale
and have usually part or all of the
intestines and reproductive tract
missing.

Poor thriving in chicks and poults

309
309 Failure to thrive as a result of
adverse environmental conditions is a
common cause of death at 5-7 days of
age. The pectoral musculature is very
thin in this chick.

108
 3 10
310 The gizzard is empty and s tained
with bile. An abnormally pale liver
contains a distended gal l bladder.
Yolk sac absorption is usually
advanced.

311 Although the quantity of fat

within the liver of birds under one
week of age is normall y high, hepatic
sections from specimens that have not
thrived reveal an excc:ssive amount of
lipid. Oil red 0 .

109
Selected reading
Coutts. G.S. ( 1981) Poultry Diseases underModernManflgemem. 2nd edition, Saiga Publishing.

Gordon. R.F. &Jordan. F.T. W. (Eds) ( 1982)PouiTryDiseases, 2nd edition, Bailliere TindalL

Hofstad. M.S .. Calnek. B.W .. Helmholdt. C.F.. Reid. W.M. & Yoder, H.W. (Eds)(I978)DiseasesofPoultry ,
7th edition, Iowa State University Press.

Ill
 Index
References in thi~ index arc to Figure numbers.

·Acute. heart fai lure'. 232-235 Coligranu!oma. l l-12

Acute pectoral myopathy. 285-287 Coli septicaemia. l-7. 27. 31. 59.
Adenocarcinoma. 158- 160 Compression. ·pinal cord. spondylolisthesi~ . 289-291
Adenovirus 127 infection, I 13 Condvles. de,·iation. 260-261: erosion. 30
Air sacculitis, 102; Coli septicaemia. 1; mycoplasmosis. 70. 80 Cong~stion. carcase, Coli septicaemia. 6: car·case. erysipelas.
Air sacs. nodules. 167 48; kidney . inclusion body hepatitis. 92: lungs. sudden death
Arthritis. viral. 120- 123: staphylococcal infection . 30 synd rome. 233. 235 .237: spleen. salmonellosis. 64:
Ascaridia galli infection, 176 subcutaneou~ fat. fatty liver kidney syndrome. 217: vein;;.
Ascites. 2.fl -2-+6 congesti,·c heart failure. 2-+ I
Aspergillosis. 164-169 Coneestive heart fail ure. 24 I -246
ihpergillusfiunigaws infection , 164 Conidiophorcs. as pergillosis. 169
Atrophy. kidneys. renal fai lure. 264-266: muscles. deep Cra7y chick disease. 202-206
pectoral myopathy. 295: pancrc<L~. stunting. 27R: thymus. Crop. disquamated epithelial cells. 173: pseudo-hyphae.
~tunting . 283 174-1 75
Cryptosporidio~ is. 193
Baby chick nephropath y. 263 Curled toe paralysis. 199-20 I
l)acilliary white dian hoc:a. ~cc Salmonella pullorum Cystic dilation. O\'lduct. 305
Bacterial diseases. 1-82
Bacterial smear. intestinal contents . 38: necrmi<: enteritis. 38: . Dacrylaria J?CIIlopam infection. 170- 172
tuberculosis. 53 Deep pectoral myopathy, 293-300
BC 14 infection. 11 3 Dermanyssus gaflinae. 196
Beading. rib heads. rickets. 208 Dermatitis. gangrenous. 43-46
·Bi!! li,·er· disease. I-tO Desquamated epithelial cells. candidiasis. 173
3o~cs. dyschondroplasia. 2-+9-256: rubbery. 209: thickened Diphtheresis, infectious laryngotracheitis. 99
growth cartilage. 210 Distended. abdomen. 280: caecum, 178. 19 1; kidney tubule.
Brachial nerve. enlarged, 126 267: small intestine. l77: urete r. 266
Brain. destruction of posterior folia . 170-17 1: Di~tortcd ribs. calcium deficiency. 213-214
encephalomyelitis. 115: h> phac. 168: periva~cularcuff. 137 Do,,n_ dubbed. 198
Bronchitis. infectious. 107-11 2 Dyschondroplasia. 249-256. 261
Bronze liver. salmonellosis. 6-f
Brown lungs. salmonellosis. 63 Egg abnormalities. I 11 -112. I I 3, 237 . 306
Hur~a of Fabricius. cystic spaces. 88: enlarged. 142: Egg drop syndrome '76. 113
haemorrhage~. 85-87: hyp.!rplasticepithelium. 88: t:imeria acermlina infection. 187-188
intlarnmation. 87: swollen. 83-84; tumours. l.f I . 142. I ~4 Eimeria bnmetti infection. I R9
Bursitis . mycoplnsrnosis. 72. 76 Eimeria mar:ima infection, 186
Eimeria meleagrimiris infection. 190
Caecum. distended. 178. I 91: haemorrhagic debri;; . ISO: Eimeria necarrir: infection. I X3-185
haernorrhagic mucosa. 181-182: typhliti~. 61-62 Eimeriatenella infection. 178-182
Cakiumddicicncy. 213-'215 Em:ephalitis. aspergillosis. 168: Marck's<!isease, 137;
Candidiasis. I 73- I 75 Newcastle di~easc . I 05
Callllida albimns. 173 Encerhalomalacia . 170. 202-206
Cannibalism . 308 Encephalomyelitis. infectious avian . 114-119
Capillaria~is. 177 Enteritis. haemorrhagic. 93: necrotic. 36--+2
Capillary. intraneural. lymphocytes. 127 l:.osinophilic coagulum. Coli septicaemia. 3
Carcinomas. 158. 162- 163 Eosinophilic cytoplasmic inclusion, epithelium. fowl pox. 97
C:~rd i ohepat i<.: syndrome . 238·2~0 Epicardium. urate deposits. 270
Cartilage. growth plate. thickened. 209-2 I0 Epidemic tremor. ll.f-119
Cellulitis. fowl cholera. I 3 Epithelium . eosinophilic cytoplasmic inclusions. 97
Cerebellum. destruction of poMerior folia . 170: focal rnalacic Erysipelas. ~g-50
lesion. 205-206: gl iosis. 105; hae morrhages. 203-20.f: Er:\'Sipelothrix rlwsiopmhiae infect ion. 48-50
pcrivascularcufllng. 106 Erythroid leuko~ i ~. 149
Chromatoly!>is. central . infe<.:tious avian em.:ephalornyditi~. t:scheridtia coli infection . 1-12. 27. 31 . 59 . 107
115-116 Exudate from footpad . mycoplasmosis. 74-75
Cloaca, protrusion. 236
Clo.wridium perfringens infection. 38 . 43 Fat. subcutaneous. congested. 217
Clo.wridium septinm1 infection. 43 Fatty liver haemorrhagic syndrome. 225-23 1
Clubbeddown. 198 Fatty liver and kidney syndrome. 90 . 216-224
Coccidiosis. 178-190 Fatty li\'Cr. poorthriving. 309-311
Colibacillo~i~ . I -12 Feather abnormalities. stunting syndrome. 276: moult. 302-304

113
feet. normal. 273: pododermatitis. 301; urate deposits. 273 infectious laryngotracheitis . 101
Femur, granuloma . 52
Fihroscd pancreas, stunting sy ndro me . 277-278 Kidneys, atrophic, 264-266: congested , 92: fine lipid droplets,
'Flip-over' . 232-235 223: infl ammation, 109- 110: necrosis . 268; nephron
Focal lesions. liver, histomoniasis, 192 dilatation. 4 1: normaL 269: pale, 220: swollen. 263,265,
Folia, destruction of, dactylariosis, 170- 17 1 269: tophus fom1ation. 274-275; tumour. 151 -152: urate
Foot, sec Feet deposi ts . 270-274
Footpad. ex udate, 74-75: swollen. 73: ulcerated . 301 Kin.ky back. 288-29 J
fowl cholera. 13-21 Knemidocoptes mutw1s infection. 194
Fowl pox, 96-97
Fractured ribs . calcium deficiency, 2 14-215 Laryngotracheitis. infectious. 98-101
Fungal diseases. 164-1 75 Layer. internal. 306
Legs . paresis, 124: scaly. 194; twisted, 262: valgus deformity,
Gangrenous dennatitis. 43-46 257-26 1
Gastroc nemius tendon, ruptured . 120. 292: slipping offjo int. Leiomyoma. 16 1
259; swollen. 28 Leukosis. erythroid. 249: lymphoid . 130-131 . 136. 140- 146.
Gliosis. infectious avian encephalomyelitis. 116: Newcastle myeloid, 147-148
disease. I05 Leukosis/sarcoma virus tumours. 140- 152
Gout. visceral. 263·275 Lipid droplets. kidney. fatty liver kidney syndrome, 223: liver.
Granulation tissue. tuberculosis. 56 fatty liver haemorrhagic syndrome. 228 : myocardium, fatty
Granuloma. aspergillosis. 165: Coligranuloma. 11- 12; liver kidney sy ndrome, 224: poorthriving. liver. 3 11
tuberculosis. 52 Lice. 195
Greencarcases. 43 Liquefaction, lung, gangrenous dermatitis . 45
Gumboro disease, 1\3-89 Lisleria moJwcYtogenes infection. 47
Listeriosis. 47
Haemorrhages, bursal, infectious bursal disease, 85-87; Liver, bronzing. congestion, 42: enlarged. 58, 13 1, 140. 149,
caecum, Eimeria rene/la. 179- I 80; cerebellum, 153 : fibrinous deposi t, 164. 1-2 . 6: focal lesions, 19 1;
encephalomalacia. 203-204 ; liver, inclusion body hepatitis. haemorrhages. 90: intranuclear inclusions. 91: lipid droplets,
90; intestine, Eimeria necatri_r. 183; muscular, infectious 228. 3 11: lymphoid infiltration . 135: lymphoid tumour.
bursal disease. 89; proventricu lus. Newcastle disease. I03: 142-142: par-boiled appearance. 49: mottling. 42: necrosis.
sub-capsular, fatty liver kid ney syndrome. 219: trachea. 33-34. 60: nom1al, 23 1, 243: pale, 218: periaeinar fatty
Newcastle disease, 102 change in hepatocytes. 246: retic ulolysis. 230: rounded
Haemorrhagic enteritis. 93-95 cytoplasmic bodies. 239-240: ruptured. 225-226. 229: small,
Head, cellulitis. 13: scabbed. erysipelas. 48 242-243: tumours . 131. 135. 140. 142: urate deposits. 272
Heart, myocarditis, 47; nom1al, 221: pale, 22 1; pericarditis, I. Lu ngs. congestion. 26. 233. 235 . 237: conidophores. 169:
6;swollen. 247; tumour. 154 brown discolouration. 63: liquefaction. 45: miliary lesions,
Hepatitis, inclusion body. 90-92; vibrionic. 58 164-165: necrosis, 46. 65
' Hepatosis', 238-240 Lymphocytes . intraneural capillary. Marek's disease . 127:
Histomonas meleagridi:;, 191 -192 peripheral nerve, Marek· s disease. 128
Histomoniasis, 191-192 Lymphocytic infiltrat ion, trachea. infectious bronchitis. I08
Hjarre ·s disease. see Coligranuloma Lymphoid infiltration . liver. Marek ·s disease. 135: pancreas,
Hock joint, sy novitis. 4 , 15-1 6.28-29. 66: urate deposits. 271: infectious avian encephalomyelitis. 117-11 8: proventriculus,
varus deformity, 78 infectious avian encephalomyelitis. I 19
Hyperplastic epithelium. bursa of Fabricius. cryptosporidiosis . Lymphoid leuko~is . 130. 136, 140-1 46
193: infectious bursal disease, 88: Lymphoproliferative disease, 153- 156
Hypertrophy . kidney . 265,266,269
Hyphae, aspergillosis . 166. 168; dactylariosis. 171 Malabsorption, 276-284
Malacia, cerebell um. em:ephalomalacia, 205-206
JLT. 96, 98- 10 1 Marek'sdisease.47, 115. 124-1 39,143,176
Inclusion body hepatitis. 90-92 :Vfetabolic disorders, 198-224
Infectious avian encephalomyelitis. 11 4-119 Metaphysis, abnonnal cartilage. 255-256
Infectious bronchitis , I07 - I 12 Metastatic nodules. adenocarcinoma. 159
Infectious bursal disease. 82-89 Mottling, li ver , necrotic enteritis. 42
Infectious laryngotracheitis. 98- l 01 Moul t, 302-304
Infectious synovitis. 72-77 Mucus. blood-stained. fowl cholera. 18
Inflammation. kidney. infectious bronchitis . 109-1 10: synovial Muscles , atrophy, 295; haemorrhages, 89; necrosis , 294-300,
membrane. mycoplasmosis. 77: trachea. infectious 2X5-287: neoplastic cells, 134; normal, 299; pale. 179:
bronchitis, 107; wingjoint, mycoplasmosis . 76: bursa of proliferating rnyelocytes. 14X; tumour, 130; red, 241
Fabricius, infectious bursal disease, 87 ' Mushy chick disease', 24
Inlet, thoracic. granulation tissue, 55-56 Mycobacterium aviwn infection. 5 1-57
Internal layer, 306 Mycoplasma galfisepticum infec tion, 68-7 1
Intestine, pale, stunting. 280: small, sec Small intestine Mycoplasma meleagridis infection. 6. 78-82
Intranuclear inclusions. li ver. incl usion body hepatitis, 9 1: Mycoplasma synoviae infection, 72-77
intestine and spleen. haeri1orrhagic enteritis . 94-95: trachea. Mycoses. 164- 175

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Myelocytes, proliferating. myeloid leukosis. 148 Newcastle disease, 102; fowl cholera, 19-2 1
Myelocytoma. myeloid leukosis, 147 Pododermatitis, plantar. 302
Myeloid leukosis, 148- 149 Poorthriving, 309-3 11
Myocarditis. listeriosis. 47 Pox. fowl, 96-97
Myocardium. fat droplets. 224 Prolapse, oviduct, 307
Y1 yopathy. acute pectoral. 285-287; deep pectoral. 293-300 Protrusion, cloaca. sudden death syndrome, 236
Proventriculus, haemorrhages. 103; lymphoid infiltration, 119;
Neck. cellulitis. 13; paralysis. 138 swelling, 282
Necrosis. kidney. renal failure . 268: liver. salmonellosis. 60; Pseudo-hyphae. candidiasis. 174-175
liver. staphylococcal infection. 33-34: lung. gangrenous Pseudomonas aerugbwsa infection. 153
dermatitis. 46. 1ung. salmonellosis. 65: muscle. pectoral Pyknosis, Ylarek ·s disease, 136
myopathy, 294-300. 293-300: mucosa. small intestine.
coccidiosis. 189; necrotic enteritis 36-40 Red. liver. erythroid leukosis. 149: congestive heart failure.
Necrotic enteritis. 36-42 241
Neoplasia. 126- 136. 140-152. 153-156 . 157 Red mire. 196
Nephritis, 109-1 10. 263 . 267 Renal failure. 263-275
Nephroblastoma. IS 1-152 Reovirus infection. 28, 120- 123
Nephron dilation. necrotic enteritis. 41 Reticulo-endotheliosis virus-induced tumurs. 157
Nerve. brachial. enlarged. 126; sciatic, normal. 125: sciatic , Rcticulolysis, fatty liver haemorrhagic syndrome, 230
Schwann cell proliferation. 20 I Riboflavin deficiency. 198-20 I
Neuron. brain stem. central chromatolysis. 116 Ribs, distOited, 213-2 14: fractu red. 215: tumours, 147; rickety
Newcastle disease. I02- 106. 115 rosary. 207
Nodules. air sacs. aspergillosis. 167 Rickets. 267-2 12; stunting. 284
Normal. foot. 274: heart. 221; kidney. 269: liver. 23 1. 243; Roughened mucosa. small intestine. 187
muscle. 299; pancreas. 277; sciatic nerve. 125 Round heart disease. 247-248
Northern fow l mire. 197 Rounded cytoplasmic bodies. liver. cardiohepatic syndrome.
Nutritional deficiencies. 198-224 239-240
Ruptured. gastrocnemius tendon. 120. 292: liver. fatty liver
Oedma, lungs. sudden death syndrome. 233. 235: trachea. haemorrhagic syndrome, 225-226. 229: spleen, Marek's
Newca~tle disease. I04 disease. 129
Omphalitis. 22-27
Opisthotonos. encephalomalacia. 202 Salmonella gallinarum infection. 63-64
Orange-brown, mucus. small intestine. coccidiosis. 186 Salmonella pullorum infection. 65-67
OmirhonysstL~ syl1•iarwn. 197 Salmonella f)phimurium infection. 59-62
Osteomyelitis, staphylococcal infection. 31 -32 Salmonellosis. 59-67
Osteopetrosis. ISO Salpingitis. Colibacillosis. 5. 8-10
Ova, degenerate. 67 Scabbed head. erysipelas. 48
Ovary. degenerate ova. 67; moult. 303 Scaly leg. 194
Oviduct, carcinoma, 158; cystic dilation. 305: leiomyoma. 161 : Schwann cell proliferation. riboflavin deficiency. 200
prolapse. 307; salpingitis. 5, 8- 10 Sciatic nerve. discoloured. 200: normal. 125: Schwann cell
proliferation. 201
Pale, heart. fatty liver kidney syndrome . 22 1: kidney. fatty liver Septicaemia. coli. sec Coli septicaemia
kidney syndrome, 220; liver. fatty liver kidney syndrome . Shell. egg. abnormal. Il l . 11 3
218; muscles,coccidiosis, 179 Sinuses. infraorbital. M. gallisepticum. 68-69
Pancreas, fibrosed , 277-279; lymphoid infiltration, 11 7- 118: Skin, squamous cell carcinoma. 162- 163: tu mour. 132; wet,
normal, 277 infl amed, 43-44
Paralysis. toes, 199; transient. 138-139 Small . liver. congestive heart fail ure, 242-243
Parasitic diseases. 176- 197 Small intestine. dark contents. 222; distended . 183 . 190:
Parathyroid, enlargement, rickets , 2 12 necrosis. 36-40. 189: orange-brown mucus. 186; pale and
Paresis, :vtarek 'sdisease. 124 distended, 177; parasitism of epitheli um. 188: roughened
Pasteurella multocida infection, 13-21 mucosa. 187
Periacinar fatty change, hcpatocytes. congestive hean failure . Spinal cord. compression. 289-29 1: encephalomyelitis, I IS
246 ·Spleen. congestion. 6. 64; eosinophilic coagulum. 3:
Pericarditis, Coli septicaemia. I. 6 intranuclear inclusions. 95: tumours. 129. 153
Perihepatitis, Coli septicaemia. I Spondylolisthesis. 288-291
Peripheral nerve. lymphocytes and plasma cells. 128 Squamous cell carcinoma. 162-163
Peritonitis. Coli bacillosis. 7: fowl cholera. 17 Staphylococcal infection. 28-35.45. 76
Perivascular cuffing. :'vfarek ·s disease. 137. 139: Newca~tle SrapltYlococcus aureus infection. 28-35
disease. 106 Sternum. bursitis. 72: tumour. 147: twisted. 213
Persistent ri!!ht oviduct. 305 Streptococcal infection. 35
Pharynx, po'X lesions. 96 Stunting syndrome. 276-283
'Pink disease'. 217 Sudden death syndrome . 232-235. 236-237
Plantar pododermatitis. 30 I Swollen. see Hypertrophy
Pneumonia, aspergillosis . 164: mycoplasmosis. 70-71: Synovial membrane. inflamed. 77

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Synovitis, Coli septicaemia, 4; fow l cholera, 15-16; infectious, Typhlitis, salmonellosis, 6 1-62
72-77; salmonellosis, 66; staphy loccocal infection, 28-29,
33 Urate deposits, epicardium . 270; foot, 273; hock joint, 27 1;
kidneys 263 , 274-275; liver. 272
Tail, paralysis , 138 Ureter, distended , 266
Tarsometatarsus, dyschondroplasia , 254; enlarged, !50; Urolithiasis, 264-268
shortened, 79; varus deformity, 253
Tenosynovitis, viral, 120-123 Valgus defom1ity oflegs, 257-26 1, 262
Thickened growth plate cartilage . rickets, 210-211 Varus deformity, hock joint, mycoplasmosis, 78;
Thymus , atrophy, stunting, 282 tarsometatarsus, dysch ondroplasia, 253
T ibiotarsus, dyschondroplasia, 249-252; erosion of condyles, Veins. congestion , 241
30, 123; osteomyelitis, 3 1-32 Vibrionic hepatitis , 58
Toes, paralysis, 199 Villus, intestinal, neoplastic lymphoid cells, 133
Tophus formation, kidneys, visceral gout, 274-275 Viral arthritis. 120-123
Trachea, diphtheresis, 99-100; haemorrhages, 102; Viral diseases, 83- l 57
inflammation , 107; lymphocytic infiltration , 108; oedem a, Visceral gout, 270-272 , 274-275
104 Vitami n D deficiency , 207-210
Transient paralysis, 138-139
Tuberculosis, 5 1-57 Wattles, swollen , 13-14
Tubule. kidney. dilated, 267 Wet skin. gangrenous dermatitis. 43-44
Tumours, see Neoplasia Wing joini: inflamed 76 .
' Turkey syndrome '65' , sec Mycoplasma meleagridis infection
Twisted, leg, 257-261, 262; sternum, cage layer fatigue, 2 13 Yolk sac infection. 22-27

116