sUDIES ON PATTERNS AND TRENDS OF

POULTRY DISEASES ON COMMERCIAL

POULTRY FARMS OF SINDH

211THESIS

l

<3-A

or rro z/o,

4K

By

5HAHZADO MALKANI

Department of Poultry Husbandry

Ity of Animal Husbandry and Veterinary Sciences

IDH AGRICULTURE UNIVERSITY TANDO JAM19 9 5

IES ON PATTERNS AND TRENDS OF POULTRY DISEASES

ON COMMERCIAL POULTRY FARMS OF SINDH

Hy

SHAHZADO iMALKAM

SUBMITTED THROUGH THE DEPARTMENT OF POULTRY HUSBANDRY,

TY OF ANIMAL HUSBANDRY AND VETERINARY SCIENCES TO SINDH

AGRICULTURE UNIVERSITY. TANDO JAM

IN CONNECTION WITH THE FULFILMENT

OF THE REQUIREMENTS

FOR

THE DEGREE OF

DOCTOR OF PHILOSOPHY

IN

POULTRY HUSBANDRY

TANDO JAM. SINDH

1095

i

TABLE OF CONTENTS

PARTICULARS PAGE NO.IS

L CERTIFICATE BY SUPERVISORY COMMITTEE

ELEASEFORM

LEDGEMENTS

V

VI

VII

IXABLES

JGURES

APPENDICES

X

XVI

XVIIT

RODUCTION I

3VIEW OF LITERATURE

BACTERIAL DISEASES ...

I Salmonellosis

2. Chronic Respiratory Disease

.3. Colisepticaemia

4. Fowl Cholera

.5. Infectious Coryza

.6 Fowl Typhoid

3

3

9

II

1 1

13

14

VIRAL DISEASES 16

16. I. Fowl Pox

.2. Gumboro Disease

.3. Lymphoid Leukosis

.4. Marek's Disease

:,5. Newcastle Disease

:.6. Angara Disease (Hydropericardium Syndrome)

IS

26

29

35

40

II

[

PARASITIC DISEASES 41

I. Coccidiosis 41

<

fERIALS AND METHODS 43

Source of Data

Postmortem Examination

Rapid Whole Blood Agglutination Test

Rapid Serum Agglutination Test

1. Flate Plate Method

Agar Gel Precipitation For Marek’s Disease

I. Dish Method

1, Slide Glass Method

Hemagglutination - Inhibition Test...

1 . Materials

2. Determination of Titer of Hemagglutination Antigen

>. Standard Method

Bird Inoculation Test

Analysis of Data

I. Yearly Disease Outbreaks

2. Seasonal Disease Outbreaks

V Time Space Clustering

4. Morbidity. Mortality, and Case Fatality Rates

43

43

45

46

46

46

47

4S

48

49

51

51

52

52

52

52

54

54

iULTS AND DISCUSSION 56

Educational Level of the Poultry Farmers

Age Structure of the Poultry Farmers

Number of the Poultry Farms, Flocks and the Birds on Poultry Farms .

56

58

61

BACTERIAL DISEASES 64

I. Salmonellosis 64

III

?

Chronic Respiratory Disease

Colisepticaemia...Fowl Cholera

Infectious Coryza

Fowl Typhoid

75

84

94

103

112

VIRAL DISEASES 120

Foul Pox 120

Gumboro Disease

Lymphoid Leukosis ...

. Marek’s Disease

132

141

153

Newcastle Disease 167

. Angara Disease (Flydropericardium Syndrome) . 186

PARASITIC DISEASES 194

. Coccidiosis 194

MARY

JCLUSIONS & RECOMMENDATIONS

212

215

ENDICES .... 218

£RATURE CITED 233

IV

I

Dedications

CI dedicate this humble ejjorts,

thejruit oj thoughts and stuffy

to

mT aJJectÿonate parents who

inspiredme to higher ideals of fije.

f

)IES ON PATTERNS AND TRENDS OF POULTRY DISEASES

ON COMMERCIAL POULTRY FARMS OF SINDH

f

By

SIIAIIZADO MALKAN!

(ified that the work embodied in this manuscript has not previously been done and the)cen prepared in accordance with the thesis manual of Sindh Agriculture University,to the satisfaction of the supervisory committee.

L\Dr. Ghous Bakhsli Isani,

Professor and Dean,Faculty of Animal Husbandryand Veterinary Sciences,Sindh Agriculture University,Tnndo Jam

sor

Dr Jainiluddin Warsy,Associate Professor and Chairman,Department of Dairy Technology,Faculty of Animal Husbandryand Veterinary Sciences,Sindh Agriculture University,Tando JaijL,

jrvisor- I

Dr. Gul Mohammad Baloch,

Associate Professor and Chairman,Department of Animal Nutrition,Faculty of Animal Husbandryand Veterinary Sciences,Sindh Agriculture University,Tando Jam.

rvisor -II

.

I

Date of Thesis Defence o 9 1995.

V

!

*)H AGRICULTURE UNIVERSITY, TANDO JAM.

"THESIS RELEASE FORM"

MALKANI, hereby authorize Sindh Agriculture

iversitv. Tando Jam to supply copies of my thesis to libraries or

ividunls upon requests

'Signature

2.%- \£ .199S'

Dale

:VI

1

ACKNOWLEDGEMENTS

praise anil (/loryfor (iod - Almighty the Clierisher, the Sustainer,

and the Lordof the worlds".

ise lie to Almighty ALLAH who created man, gave him the gift of expression andm The Holy QUR'AN, which is a source of advice, healing guidance and mercy fore faith.

before Almighty ALLAH, and express my humblest and sincerest words ofIM. who bestowed upon the feeble author the potential and ability to make material> the already existing ocean of knowledge

thor of thesis feel great pleasure and honour and desires hereby to acknowledge it’so the superv isor and teacher Professor Dr. Ghous Bakhsh Isani Dean of the Facultysbandry & Veterinarv Sciences. Sindh Agriculture University, Tando Jam for hisd guidance during the conduct of research work Wish profound gratitude and deepion. I wish to thank him and I find no words to express my immense gratitude foriggestions. inspiring guidance, personal interest without which, this thesis wouldaineil it’s present shape and it is a matter of great pride and privilege for me to

elings of obligation and deepest indebtedness to my supervisor Dr Isani for hisking guidance and encouraging attitude during the entire study programme. I foundand politely behaving during my period of study and I pray for his success in Din

I for his good health

also wishes to express his sincere feeling of thanks to the members of supervisoryJamiluddin Warsy, Associate Professor and Chairman. Department of Dairy

id Dr Gul Mohammad Baloch. Associate Professor and Chairman. Department ofon for their keen cooperation and valuable suggestions and sincerest appreciationsled to Mr Noor Nabi Ansari. Associate Professor and Chairman, Department ofndry and Mr. Muhammad Akbar Arain. Assistant Professor, Department of Dairyr their cooperation.

o the author's profound privilege to express his sincere thanks to Dr. Bashir Ahmedman. Pakistan Science Foundation. Islamabad for his great help in printingf lesions from PSF, the author is deeply indebted to him and his staff who assisted

: great pleasure to the author in expressing great debt of the sincerest gratitudes to

>ar Malik, Director. Advanced Studies and Research. Sindh Agriculture University.

>r his valuable suggestions for the improvement and standardization of the

operation extended by Dr. Shaft Muhammad Niznmani, Professor, Faculty of Cropidh Agriculture University. Tando Jam for his guidance in statistical analysis of thely acknowledged.

VII

:r

r

Uithor cannot forget the cooperation and facilities provided by Dr. Hisao Bamba,department poultry research institute health division Aichi Agricultural Researchiecial member of the Japanese society of poultry diseases, for his help in teaching me

ds of diagnosis of poultry diseases and in collection of references during my trainingin.

also wishes to extend his thanks to Mr. Abdul Majeed Soomro, Senior Clerk,

>1“ Livestock Management for typing this thesis with care and patience. He haswith the author in every' movement of struggle I pray for his success in life.

s are due to Mr. Sliafique Ahmed. Photographer for preparation of slides and authoril to Mr. Ehsan Ali Qazi for his contribution in analysis of data on computer.

ilhor is indebted to his sons Zulfiqar Ali Malkani and Musharaf Ali Malkani for theiri references and tabulation of the data The author inspired his sons to higher ideals

SNAHZADO MALKANI

VIII

!

LIST OF TABLES

PAGE NO.PARTICULARS

Educational level of poulry farmers. 57

Age structure of poultry farmers. 59

Number of the poultry farms, flocks and the birds on poultry farms 62

Morbidity, Mortality and Case Fatality rates in different diseasesreported on commercial poultry farms of Sindh during 15 years.. 63

Analysis of variance of data on outbreaks of various diseasesin Karachi 208

Analysis of variance of data on outbreaks of various diseasesin Hyderabad 208

Analysis of variance of data on outbreaks of various diseasesin Nawabshah 209

Analysis of variance of data on outbreaks of various diseasesin Mirpurkhas 209

Analysis of variance of data on outbreaks of various diseasesin Sanghar 210

Morbidity and ranking of the diseases according to their

irnpoilance and research priority 210

IX'

'

i

LIST OF FIGURES

PARTICULARS PAGE NO.

iber of outbreaks of Salmonellosis in Sindh

cal lesion of arthritis in Salmonellosis..oidily of ovary in Salmonellosis

r with pin point necrotic foci in Salmonellosis

ds of Salmonellosis on poultry farms of Karachi

ds of Salmonellosis on poultry farms of Hyderabad

ds of Salmonellosis on poultry farms of Nawabshah

ds of Salmonellosis on poultry farms of Mirpurkhas

ds of Salmonellosis on poultry farms of Sanghar

iber of outbreaks of Chronic respiratory disease in Sindh

;ac intlammation in Chronic respiratory disease

-membrane intlammation in Chronic respiratory disease

ds of Chronic respiratory disease on poultry farms of Karachi

ds of Chronic respiratory disease on poultry farms of Hyderabad

ds of Chronic respiratory disease on poultry farms of Nawabshah

ds of Chronic respiratory disease on poultry farms of Mirpurkhas

ds of Chronic respiratory disease on poultry farms of Sanghar

iber of outbreaks of Colisepticaemia in Sindh

•re pericarditis, perihepatitis and airsacculitis in Colisepticaemia

:arditis and perihepatitis with white deposits on the heart and on the liver

jlisepticaemia

r showing severe hepatitis with urate deposits in Colisepticaemia

e deposition on the heart and on the liver in Colisepticaemiated chicken

65

66

66

67

69

70

71

72

73

76

67

77

79

SO

8!

82

83

85

77

86

86

87

X

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f

illen and congested liver with severe hemorrhagic spots due to E.coli.

nds of Colisepticaemia on poultry farms of Karachi

nds of Colisepticaemia on poultry farms of Hyderabad

nds of Colisepticaemia on poultry' farms of Nawabshah

nds of Colisepticaemia on poultry frams ofMirpurkhas

nds of Colisepticaemia on poultry' farms of Sanghar

liber of outbreaks ofFowl cholera in Sindh

low nodules, white necrotic lesions and hemorrhages on the liverand pin-point hemorrhages on the heart (B) in Fowl cholera

lominal fat with hemorrhagic lesions in Fowl cholera .

nds of Fowl cholera on poultry farms of Karachi

nds of Fowl cholera on poultry farms of Hyderabad

nds of Fowl cholera on poultry farms of Nawabshah

nds of Fowl cholera on poultry farms of Mirpurkhas...

nds ofFowl cholera on poultry' farms of Sanghar

tuber of outbreaks of Infectious coryza in Sindh

elling of the face and wattles in Infectous coryza

t swelling of the eyes, face and sinuses in Infectious coryza

:nds of Infectious coryza on poultry farms of Karachi

:nds of Infectious coryza on poultry farms of Hyderabad

of Infectious coryza on poultry farms of Nawabshah

mds of Infectious coryza on poultry farms of Mirpurkhas

mds of Infectious coryza on poultry farms of Sanghar

mber of outbreaks ofFowl typhoid in Sindh

mds of Fowl typhoid on poultry farms of Karachi

mds of Fowl typhoid on poultry farms ofHyderabad

_‘nds of Fowl typhoid on poultry farms of Nawabshah

mds of Fowl typhoid on poultry farms of Mirpurkhas

mds of Fowl typhoid on poultry farms of Sanghar

unber of outbreaks ofFowl pox in Sindh

87

89

90

91

92

93

95

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96

97

9S

99

100

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107

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1 13

114

115

1 16

1 17

118

121

XI

t

ms of cutaneous form of Fowl pox

ing symptom in membranous form of Fowl pox

bination of cutaneous form and membranous form in Fowl pox

ation in larynx in Fowl pox

ers imbedded in the membranes of mouth, throat and windpipe in wet

of Pox

vn scabs start as small, rapidly growing white bumps in "dry pox"

ds ofFowl pox on poultry farms of Karachi

ds of Fowl pox on poultry' farms of Hyderabad

ds of Fowl pox on poultry farms of Nawabshah

ds of Fowl pox on poultry farms of Mirpurkhas

ds of Fowl pox on poultry' farms of Sanghar

iber of outbreaks of Gumboro disease in Sindh

Hen bursa of Fabricius containing a yellow cheesy material in

iboro disease

ids of Gumboro disease on poultry farms of Karachi

ids of Gumboro disease on poultry farms of Hyderabad

ids of Gumboro disease on poultry farms of Nawabshah

ids of Gumboro disease on poultry farms of Mirpurkhas

ids of Gumboro disease on poultry farms of Sanghar

iber of outbreaks of Lymphoid leukosis in Sindh

iptoms of Lymphoid leukosis in adult chicken

use morbidity of liver in Lymphoid leukosis

ed morbidity of liver in Lymphoid leukosis

•bidity of kidney in Lymphoid leukosis

bidity of Fabricius bursa in Lymphoid leukosis

bidity of ovary in Lymphoid leukosis

ids of Lymphoid leukosis on poultry farms of Karachi

ids of Lymphoid leukosis on poultry farms of Hyderabad

nds of Lymphoid leukosis on poultry farms of Nawabshah

ods of Lymphoid leukosis on poultry farms of Mirpurkhas

122

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129

130

133

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135

136

137

138

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142

134

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145

147!

148

|149

150

XII

r

s of Lymphoid leukosis on poultry farms of Sanghar

er of outbreaks of Marek's disease in Sindh

aralysis in classical Marek's disease

paralysis in classical Marek's disease

-sis of the legs and neck in classical Marek's disease affected bird

idity of sciatic nerve in classical Marek's disease

iditv of ovary in classical Marek’s disease

toms of acute Marek's disease in badly affected bird

idity of viscera in acute Marek's disease

idity of liver in acute Marek's disease

idity of heart in acute Marek's disease

idity of lung in acute Marek's disease

idity of skin in acute Marek's disease

is of Marek's disease on poultry farms of Karachi

Is of Marek's disease on poultry' farms of Hyderabad

Is of Marek's disease on poultry farms of Nawabshah

Is of Marek's disease on poultry farms of Mirpurkhas

is of Marek's disease on poultry farms of Sanghar

her of outbreaks of Newcastle disease in Sindh

len kidneys and hemorrhages in the proventriculus of Newcastle diseaseted chicken

shaped ovaries in Newcastle disease

shaped ovaries in Newcastle disease affected hen

entriculus showing very marked and characteristic hemorrhagic lesions’wcastle disease

plete or partial paralysis of the wings and legs of nervous system

ted bird in Newcastle disease

iorrhages in the proventriculus in Newcastle disease

liratory symptom of Newcastle disease

entriculus of Newcastle disease

en in Newcastle disease

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145

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172

173

XIII

fssue in Newcastle disease (N.D)

pipe of ND (The left side shows the cloudiness of mucous>rane and the increased mucus, and the right side shows hyperemialeeding)

idity of ovary in Newcastle disease

1 patches and hemorrhage in proventriculus and small intestine inlenic Viscerotropic Newcastle disease (VVND)

: intestine of VVND affected chicken with blood patches

1 patches and necrosis of the cecal tonsils in advanced case of VVND...

;sive fluids are commonly seen in the respiratory tract in VVNDed bird

ictivitis and edema of the eyelids (VVND)

>rrhage in the mucosa of the trachea (VVND)

Is of Newcastle disease on poultry farms of Karachi

Is of Newcastle disease on poultry farms of Hyderabad

Is of Newcastle disease ori poultry farms of Nawabshah

Is of Newcastle disease on poultry farms of Mirpurkhas

Is of Newcastle disease on poultry farms of Sanghar

jer of outbreaks of Hydropericardium in Sindh

Is of Hydropericardimn on poultry farms of Karachi

is of Hydropericardium on poultry farms of Hyderabad

Is of Hydropericardium on poultry farms of Nawabshah

Is of Hydropericardium on poultry farms of Mirpurkhas

Is of Hydropericardium on poultry farms of Sanghar

ber of outbreaks of Coccidiosis in Sindh

I intestine lesions in chronic Coccidiosis

d in small intestine and large intestine with characteristic swelling inidiosis

len caeca filled with a bloody mass in caecal Coccidiosis

orrhage on the caecal tonsils, small intestine and other organs in caecalidiosis

a of a pullet distended with blood in E.tenella Coccidiosis

173

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176

176

177

177

179

ISO

ISI

1S2

IS3

1S7

189

190

19!

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193

195

196

196

197

197

198;

XIV

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stage of Eimeria tenella infection. Caeca contains pink and white cores,

led from blood cells, plasma, tissue debris

nella caeca with bloody mass due to blood vessels hemorrhaging in>rgan

nella Coccidiosis, caeca swollen and filled with a bloody mass

aining lymph, tissue cells and other debris

racteristic swelling of small intestine in E.necatrix (Coccidiosis)

,*rely swollen intestine filled with blood in E.necatrix (Coccidiosis)

ew of a portion of upper half of intestine showing whitish patches, the

ilt of light infection in E.acervulina Coccidiosis

ng of the intestine being bright red in a heavy E.acervulina (Coccidiosis).

ids of Coccidiosis on poultry farms of Karachi

ids of Coccidiosis on poultry farms of Hyderabad

ids of Coccidiosis on poultry farms of Nawabshah

ids of Coccidiosis on poultry farms of Mirpurkhas

ids of Coccidiosis on poultry farms of Sanghar

198

199

199

200

200

201

201

203

204

205

206

207

XV

LIST OF APPENDICES

PARTICULARS PAGE NO.

Monthwise number of outbreaks of various diseaseson commercial poultry farms of Sindh for the year I97S

Montlnvise number of outbreaks of various diseaseson commercial poultry farms of Sindh for the year 1970

Monthwise number of outbreaks of various diseaseson commercial poultry farms of Sindh for the year I9S0.

Monthwise number of outbreaks of various diseaseson commercial poultry farms of Sindh for the year IOSI

Monthwise number of outbreaks of various diseaseson commercial poultry farms of Sindh for the year I9S2

Monthwise number of outbreaks of various diseaseson commercial poultry farms of Sindh for the year I9S3

Monthwise number of outbreaks of various diseaseson commercial poultry farms of Sindh lor the year 1 0S4

Monthwise number of outbreaks of various diseaseson commercial poultry farms of Sindh for the year I9S5.

Monthwise number of outbreaks of various diseaseson commercial poultry farms of Sindh for the year 1086.

Monthwise number of outbreaks of various diseaseson commercial poultry farms of Sindh for the year I9S7.

Monthwise number of outbreaks of various diseaseson commercial poultry' farms of Sindh for the year 1088

Monthwise number of outbreaks of various diseaseson commercial poultry' farms of Sindh for the year 1089.

Monthwise number of outbreaks of various diseaseson commercial poultry farms of Sindh for the year 1090.

Monthwise number of outbreaks of various diseaseson commercial poultry farms of Sindh for the year 1901.

Monthwise number of outbreaks of various diseaseson commercial poultry farms of Sindh for the year 1902.

2 1 S

210

220

221

222

223

224

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225

226

10.

227

228

229

13

230

14

231

15

232

XVI

i

AN ABSTRACT OF THE THESIS OF

forShahzado Malkani

Major: Poultry Husbandry

dies on patterns and trends of poultry diseases on commercial poultry farms>indh.

h the data available at poultry disease diagnostic laboratories in various districts of:he data collected during survey was analysed to study the pattern and trends of poultry

immonly occurring on commercial poultry farms of the province. These laboratoriesing in Karachi, Hyderabad, Nawabshah, Mirpurkhas and Sanghar.* Thirteen major.eases i e. Salmonellosis, Chronic respiratory disease, Colisepticaemia, Fowl cholera,

coryza. Fowl typhoid. Fowl pox. Infectious bursal disease, Lymphoid leukosis, Marek's

ewcastle disease, Angara disease and Coccidiosis, were diagnosed during the study. In

Salmonellosis was reported from 1328 farms. Chronic respiratory disease from 636

isepticaemia from 470 farms. Fowl cholera from SI farms. Infectious coryza from 463

vl typhoid from 4! farms. Fowl pox from 55 farms. Infectious bursal disease from 148

nplioid leukosis from 520 farms, Marek's disease from 309 farms, Newcastle diseasefarms, Angara disease from 223 farms and 1216 farms were affected with Coccidiosis

;l number of outbreaks of Salmonellosis, Chronic respiratory disease, Colisepticaemia,era, Infectious coryza. Fowl typhoid. Infectious bursal disease. Lymphoid leukosis,

sease. Newcastle disease, Angara disease and Coccidiosis were reported from Karachiwest being from Sanghar; but in case of Fowl pox. the highest number of outbreaksrted from Sanghar and the lowest from Mirpurkhas. Analysis of variance of data on

of various diseases showed non-significant difference, amongst diseases and years inMirpurkhas and Sanghar districts. Hyderabad and Nawabshah showed significant

mongst diseases and non-significant variance amongst years. The morbidity rate per

15.7S8 percent for Salmonellosis, mortality rate per farm was S.274 percent and case

e averaged 14.763 percent. The morbidity rate per farm was 23.995 percent for Chronic

/ disease, mortality rate per farm was 11.181 percent and case fatality rate averagedrcent. The morbidity rate per farm was 1 1.85 percent for Colisepticaemia, mortality rate

.vas 5.25 percent and case fatality rate averaged 12.84 percent. The morbidity rate per

20.16 percent for Fowl cholera, mortality rate per farm was 9.14 percent and case

ite averaged 23.473 percent. The morbidity rate per farm was 20.67 percent for

coryza, mortality rate per farm was 10 percent and case fatality rate averaged 15.625

’he morbidity rate per farm was 9.70 percent for Fowl typhoid, mortality rate per farm

percent and case fatality rate averaged 25.08 percent. The morbidity rate per farm was

cent for Fowl pox, mortality rate per farm was 10.97 percent and case fatality rate

22.225 percent. The morbidity rate per farm was 19.74 percent for Infectious bursallortality rate per farm was 9.44 percent and case fatality rate averaged 21.53 percent.

>idity rate per farm was 20.36 percent for Lymphoid leukosis, mortality rate per farmi percent and case fatality rate averaged 20.23 percent. The morbidity rate per farm was

cent for Marek's disease, mortality rate per farm was 12.254 percent and case fatality

XVII

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cl 25 49 percent The morbidity rate per farm was 24.75 percent for Newcastletalitv rate per farm was also 24 75 percent and case fatality rate averaged 34.61

• morbidity rate per farm was I 1.54 percent for Angara disease, mortality rate per

17 percent and case fatality rate averaged 12.72 percent and the morbidity rate per

' 55 percent for Coccidiosis. mortality rate per farm was 14 IS percent and case

iveraged 22 94 percent. The study of diseases showed similar pattern of occurrences

tricts. The diseases like Salmonellosis, Chronic respiratory disease. Colisepticaemin,i. Infectious coryza. Fowl pox. Infectious bursal disease. Lymphoid leukosis, Marek's

.castle disease. Angara disease and Coccidiosis showed a rising trend on commercialis of Sindh, whereas Fowl typhoid showed a secular trend In this study, the socialthe poultry farmers in Sindh was also studied.

.Will

r

CHAPTER- I

INTRODUCTION

ry industry. as a source of animal proteins for a balanced human diet, occupies an

see in the sphere of food production. The two fundamental aspects of food problem

ding and malnutrition are directly related to the healthy Pakistani nationals. The

capita availability of protein from animal sources is 25 grams against the

d 3 7 grants The existing sources of meat production are not sufficient enough to

mand of present population in Pakistan. Therefore, a common man is not getting

'ding to his requirement. The shortage of proteins of animal origin can be combated

: more eggs and meat by growing more poultry. This can help in filling the gap of

ibility as the poultry has rapid growth rate and low' generation gap in comparison to

k.

ry production in the country can be divided into tw'o sub-sectors namely commercial

>-sectors. Rural units are made almost entirely of native chickens kept by people in

the contrary commercial units comprising of exotic strains are located mainly in and

s which help in increased supplies of meat and eggs. On a commercial poultry farm.

sentiallv considered as an egg and meat producing machine. The object of the poultry

lintaining and rearing the birds at his farm is to produce eggs and broilers of good

:h a low cost which may ensure reasonable margin for him and help him in keeping

:ontinuous production. Thus the broiler and the layer farming is the only cheapest

rease the production of animal protein.

poultry in Pakistan in general and that of in Sindh particular is faced with many

he most important being the problem of disease control Previously the spread of

dium Syndrome (Angara disease) created havoc in the poultry industry. Till the

not properly diagnosed, it's control became extremely difficult. Similarly, there are

>u1try diseases causing economic losses each year.

i

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1

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cry production can further be increased if treatment of diseases and their control

e continued to be strengthened on scientific lines This can not be achieved without

roper and correct diagnosis of the diseases

disease problem on the commercial poultry- farms are because of many reasons like

is are of exotic origin hence are not fully adapted to our climatic conditions.

management causes stressful conditions which lead to contraction of the disease by

e resistance of the birds, hi) proper handling and schedule of vaccination is not

the commercial farmers and iv) incorrect feeding and faulty management predispose

the diseases.

control or treatment of the diseases can not be successfully achieved until and unless a

thentic data on disease occurrences is available The data on incidences, prevalence.

terns and trends of poultry diseases on the commercial poultry farms in .Sindh are

herefore. becomes imperative to design such an study as to compose clear position

he disease occurrences on the commercial poultry sector of the province

v. the present study was designed to compose the picture about the incidences.

patterns and trends of the most commonly occurring poultry diseases on the

v operating poultry farms. The result of the present study will definitely help in

a meaningfull diagnostic and disease control policies The findings of the study will

.e extension workers in understanding the diagnosis, treatment and control of the

d will definitely help the planners to establish a disease forecasting system which is

ry much lacking in the province

V

CHAPTER- M

REMEW OF LITERATURE

TERIAL. DISEASES.

lonellosis.

onellosis (Paratyphoid) was widely recognized as a disease of economic importance

ions birds in the second and third decades of this century Not until tile middle of the

vever did it begin to come under thorough review This came about largely through

vareness that disease in man had a relation to infection in poultrv Contributing also

ve work on Salmonella typing beginning in the early I930's at the university of

nder the leadership of Dr Philip R Edwards. (Kenneth 1977) Salmonellosis in fowl

-ted as involvement with Salmonellae other than those causing - pullorum disease and

id. It became manifested earlv that Salmonella infection was widespread in birds and

icluding man. The disease was first reported in the United States in pigeons in 1895.

1920. in chickens the following year, and in turkeys in 1933, That the disease was

so in carriers and other birds in pet stores evidenced by repons from New Jersev in

from Michigan in 1929, The European literature of that period contained many

o Salmonella serotypes in digestive disturbances of man from ingestion of infected

geon eggs. With Salmonella being ubiquitous and so many new types being continually-

understanding of those infections did not develop in the orderlv fashion that

‘d Pullorum disease.

ianis and Whittemore (1976) used six methods in testing for prior exposure of

o Salmonella typhimurium (ST) The most sensitive and reliable was the

lobulin (MAG) test; less reliable were the tube agglutination, micro-agglutination.

a blood, and rapid serum-plate tests. Serologic detection of Salmonella infection has

jred by the low level of antibodies stimulated by the infections, and by the insensitivity

sting procedures (Yamamoto, et ah 1962; Olesiuk et ah, 1969; Sato, 1970). Official

3

&

testing programs have directed attention to only a single Salmonella serotype.

vphimurium (ST), group B The method applied most routinely for detecting ST

both turkeys and chickens under the National Poultry Improvement plan (NTMP)

. 1975) has been the macroscopic lube agglutination (T) test (Anonymous. 1971)

en and Marthedal ( 1970) reported somatic and flagellar T tests for ST to be valuable

eliminate this infection from Danish chicken flocks

the microagglutination (MA) test (Williams and Whittemore. 1971. Williams and

1972: Anonvmous. 1975) was also recognized under the NPIP as an official method

g ST infection in avian species. Some workers had reported (Williams and

1972. Williams and Whittemore. 1972. Kumar et aj . 1974) that the

jbulin (MAG) test was the most sensitive and effective method for detecting

antibodies in chickens and turkeys. The .rapid-serum-plate (SP) test for avian

infections had seldom been applied Bierer and Vickers (1960) reported the SP test

or to the T test and rapid-whole-blood (WB) test in detecting turkeys demonstrated

be carriers of ST inlection Kumar et. ah (1974) reported the SP test to be more

in the T and MA tests for turkey flocks when a new antigen with low cel!

n and low PH was used Experimental and field applications of the WB test for

iratyphoid infections in chickens have been described by Clarenburg and Romijin

atkin and Grinewitsch. ( 1955). Blaxland ei. al. ( 195 S ) and El-Agroud and Sadek

uugh Cloacal swab C-culture has been applied widely under field conditions, if s

>r detecting avian Salmonellosis seemed limited because fecal excretion of the

tight be intermittent (Wilson. 194S. Magwood and Bigland. 1962) Oiesiuk et a]

rted that culture of floor litter was more effective than serologic tests or C-culture fot

perimental ST infection Sato et ah (1970) reported the single C-culture test to be

ifforts to eliminate Salmonella infection from selected poultry flocks Athough Brown

i frequently failed to detect Salmonella infected cockerels with C-culture. early in the

isolation of ST from C-cultures was related to recovery of the organism at autopsy

Snoeyenbos (1976), used the direct culture and fluorescent antibody (FA) procedures.

ig approximately 6200 samples of poultry floor or nest litter for Salmonellae.

4

i

r - sample culturing has been shown to be a reasonably accurate and practical method

: infected flocks fSnoeyenbos et a] , 1970. Snoeyerfcos 1971) This method has in pan

d in tlie protocol of the National Poultrv improvement plan (LSDA. 1975).

.iral methods for isolating salmonellae has been considered costly and lime -

;ince 5-7 days might be required for results (Gibbs et a]., 1972, Bahl et al., 1975,

. 1975) To overcome their disadvantages, the fluorescent antibody (FA) technique

id increasingly by the food industry'. Cherry et ai i '.975) have tabulated 34 repons in

.as used to examine food and environmental samples Other investigators have used

ine turkey feces and poultry related products (Gibbs et ah. 1972: Bahl et a}.. 1975.

lal . 1975)

he early 1940's, about 60 serological types of Salmonellae had been recognized.

; isolated from fowl More than S00 serotvpes has been identified at that time B\

1700 known Salmonella serotypes has been reponed. Of these. 153 have been .

the United Stales from chickens and Turkeys Host specificity was not a common

rious species and serotvpes have been found as common pathogens in many species o'

Stic and wild animals, man. and reptiles It was not uncommon to find more that one

invoked in a single outbreak. Direct transmission of Salmonellae to man from live

: been reported occasionally. Usually, however, transfer to man has been from poultry

>ultrv byproducts. A small amount of infective material might contaminate food in a

plant and be allowed to proliferate in transit or in the kitchen through improper

le ensuing attacks were principally gastro-enteritis Poultry and poultry products were

doubtedlv a major source of contamination but were frequently accused mistakenly

ifair publicity Salmonellae have been studied more extensively in poultry' than in other

the number of isolations was greater. It was estimated that the source of infection was

in fewer than 50% of human cases. Many poultry processing plants have established

ontrol testing services to monitor Salmonel’a organisms in their operations

:ia et ah ( 1979) assessed the Salmonella status of 15 different farm flocks at the farm

processing plants. Bacteriological examination for Salmonella was made of litter.

5-dav-o!d culled chicks, and chicken carcasses Fresh straw litter was found

•d with Salmonella and was suspected to be a source of flock infection, and culture of

5 ft

Ii

a

f*

er in particular was considered a good indicator of carcass contamination at

lams Properiy peileted feed did not contain Salmonella. Processing did not render

e of Salmonella.

rv. a major food source, has long been recognized as one of the principal source of

nfections in man. A survey in Canada (Duitschaever. 1977) found a contamination

34.S9 o of retail chicken products

ih rate of Salmonella contamination of carcasses was due to contamination at the

essing plants (Timoney er rd . 1970; Simmons and Byrnes. 1972. Me Garr, 1976)

;lla serotypes found in processed carcasses and processing plant environments were

es found on broiler rearing farms (Woodburn and Stadelman 196S: Simmons and

2. Bains and Mackenzie. 1974). Timonev et a] (1970) also showed that serotvpes

n carcasses changed with the flocks being processed, and concluded that the

with Salmonella in processing plants was introduced on birds from infected flocks

eidence of Salmonella infection in poultry' was difficult to ascertain, since birds might

fected without showing clinical disease. Surveys in various countries have shown an

wing from 0 1% to 5% (Gordon. 1971)

ire of floor litter has been shown to be a reasonably accurate and practical method for

ected flocks (Olesiuk ej a] . 1969. Snoeyenbos et a!., 1969; Snoeyenbos. 1971). and

Olesiuk et ai. ( 1969), floor litter was more dependable than serological tests, cloacal

;st litter.

i new litter was found contaminated, the same serotypes were recovered from the

s collected at 5 days, at 6 weeks, also from the dust collected at 6 weeks, culled

carcasses of the same flock at the processing plant unused poultry litter has been

>e contaminated and might be a source of infection for poultry (Kumar et ah, 1971,

d Byrnes, 1972) Harvey. (1973) found 3 of 20 (15%) of fresh litter samples to be

i The same serotypes were later isolated from cloacal swabs taken from birds

d Byrnes (1972) isolated 6 serotypes from new litter (wood Shavings) before the

ilaced in the barn. Fanelli er a|. (1970) stated that litter eventually developed an

feet for Salmonella. Similarly Snoeyenbos et ai (1967) noted that older litter

6

l

i*

t

relatively high PH and was Salmonellacidal as compared with new litter. Tucker

1 that new litter remained infected only for a few days after healthy chicks were

nact with- infected litter. Out of 15 forms visited, rate of isolation was 17 ITo from

1 S% at 5 davs. and 24% at 6 weeks. Snoeyenbos et al ( 1970) found that culturing

as a reliable means of detecting Hock infection, and Olesiuk et a] (1969) obtained a

mage of isolates from floor iitter They further suggested that floor litter was more

ban serological tests, or culture of cioacal swabs, drinking water, eggs, or embryos

flock infection Snoeyenbos (1971) stated that litter samples collected at 1.3, and 5

•tarting chicks on new litter yields a dependable evaluation of the status of flocks

aminated feed may be an important source of Salmonella in poultry Snoeyenbos et al

i convincing evidence that feed contamination resulted in flock infection However.

with Salmonella has been drastically reduced (Zindel and Bennett. 196S: Harvey.

in et. al., 1974), In this study. S havana and S heidelberg were isolated from dust

the same time, it was fell that the feed might have been contaminated, by the dust.

s were collected at 5 aavs io find out whether birds were infected. 6 chicks were

ed amongst 90 culled chicks from 4 farms and the serotypes found were the same as

.T in 3 flocks. The chicks examined in this study could have been infected before

ley might have become infected from litter. On 2 of 4 occasions serotypes found in

nd once in 5-days litter were the same as those found in culled chicks. The results

at litter might be a likely source of infection.

ts been shown that processing methods were incapable of rendering carcasses

free of contamination (Hacking. 1976). In fact it has been shown that processing

minate Salmonella by cross contamination . Contamination actually was higher after

han before. Morris and Wells (1970) found flock infection to be 20% initially and

time the carcass was packed, similar rises have been reported by others (Patrick et al ,

iherty, 1974; Me Garr, 1976). Costerton el al. (1978) stated that bacteria stuck

often with exquisite specificity, to surfaces ranging from human tooth, lung, and

rock submerged in a fast - moving stream. The means of adherence was a mass of

rs of polysaccharides that extend from the bacterial surface and form a glycocalyx.

n mediated by the glycocalyx determined the particular location of bacteria in most

7

p

onments This phenomenon has been observed with a number of bacteria, e.g,.

fragilius. Stapiiyiccoccus aureus. \ ibrio cholera. Neisseria gonorrhoea. and

•phiinuriujn Perhaps that was why Salmonella, once they were firmly stuck to the

could not be washed away. Glazen et a] ( 1966) reported that 2 factors intluenced

of Salmonella contamination in a processing plant . 1 ) The equipment and method

and 2) The number of infected birds processed, Timonev et ai (1970) stated

?r docks were the main source of carcass contamination, not the plant itself

nples examined by Milakovic and Selec (1990). front various categories of 26 to

dead or diseased fowls. Salmoneilae were isolated from 0.2 to 10.10 6°-'o . Samples

o) of 394 turkeys. 4Sf 14° o) of 350 ducks. 8 (2%) of 376 pheasants. 5 { 1%) of 457

ere also positive. The predominant serotypes were S enteritidis. S. virchou and S.

in fowls. S iivingstone. S virchow. S anatum and S hedar in turkevs. and S

and S agona in isolated from 222 (8%) of 2628 liver samples and 89 (5%) of 1706

. of fowl origin and 7 (20/o) of 363 fishmeal samples

rtuary 1990 an outbreak of Salmonellosis was reported by Sergevnin et a] (1991).

'474 cases. Another outbreak occurred in Febmarc among 151 workers in a local

iter In both cases the source of infection was salad prepared by local caterers using

hen utilities as in processing poultry products.

igue et ai , (199Q) reported over the past 5 years the number of Salmoneila enteritidis

humans have increased on both sides of the Atlantic ocean. The VVHO Salmonella

data for I979-S7 were reviewed and showed that S enteritidis appeared to be

i at least the continents of North .America. South .America, and Europe, and might

:a. S. enteritidis isolates increased in 24 (69%) of 35 countries between 1979 and

79. only 2 (10%) of 21 countries with data reported S. enteritidis as their most

monella serotype, in I9S7. 9 (43%) of 2 1 countries reported S enteritidis as their

>n serotype; 8 (S9%) of 9 were European countries Although the reason for the

se was not yet clear, investigations in individual countries suggested it was related to

of eggs and poultry which harboured the organism

I

I1

i

S

i

'

»

inic Respiratory Disease (CRD).

tplasma gallisepticum (MG') was of continuing economic concern in all areas of the

;s (Yoder. 1 MS 4 ) Vaccination of replacement commercial layer pullets with a killed

ive culture of MG has been used to reduce egg production losses, medication costs.

v associated with exposure to field strains of MG (Carpenter et ah. 1981, Glaisson

I°84. Kleven et aj 1984. Voder e; ai . I°S4j it has been demonstrated that

with an oil emulsion bacterin did not adequately protect against tracheal colonization

der et a], i9$4: Talkington and Kleven. 1985). nor did it significantly reduced the

organisms in the tracheas of infected chickens (Kleven. 1985). Similar works with the

has demonstrated that vaccination with F strain significantly lowered the isolation rate

ic MG strains from the tracheas of heavily challenged birds (Levisohn and Kleven.

jplasma gallisepticum (MG) was considered a significant pathogen of chickens and

momic losses from MG infections resulted from mortality, reduced weight gain and

cv. decreased egg production, and increased condemnations Various antibiotics such

he tetracyclines, spectinomvcin and lincomycin have been used to minimize losses

1G (Olson et al . !9c>0: Olesuik et al . 1964; Hamdv and Blanchard. 1969. Ose el a] .

)hn. 1981)

commonly employed treatments that tended to provide favorable results included

xytetracvcline. chlonetracvcline (CTC). or tylosin in the feed (Yoder. 1984). Tylosin

monstrated to slow transmission of MG as well as to improve production and feed

experiments infected birds (Ose et ah. 1979) Olesuik et ah (1964) reached similar

concerning the effectiveness of medication with potentiated CTC and oxytetracycline

ulated chickens, despite these and other repons on the value of antibiotic feed

n treating iVIG-infected.

aplasma gallisepticum (MG) was considered one of the costliest disease agents in the

layer industry. It has been estimated tiiat MG - infected hens produced nearly 16

ter bird than uninfected hens, resulting in a potential annual financial loss to the V.S.

v of SI 18 million (Carpenter £t ah. 1979; Carpenter et. ah, 1981).

9

*

»

*0

limson and Rosenstein (1976) studied two chicken breeding flocks from different

les serologically and culturally' for Mycoplasma gailisepticum (MG) throughout their

d laying period in California. The prevalence of Mycoplasma gailisepticum (MG) and

a synoviae (MS) in commercial pullet and layer flocks in southern and centra'

was estimated by testing serum and egg-volk samples from 360 sample flocks in

ilifnrnia and 41 sample flocks in central California The estimated true prevalence rate

is 73° o in southern California and 3% in central California. The estimated true

rate of MS was 91% in southern California and 32% in central California. Compared

cted flocks, MG - infected flocks in southern California were significantly older anti

ated less (P<0.05) More managements were under a multiple age system, more flocks

, more were vaccinated with F-Strain, and more had concurrent infection with MS

ily one sample flock in central California was MG-Infected none were vaccinated with

recent study in Pennsylvania showed that Mycoplasma gailisepicum (MG) in

i layers contributed to significant economic losses (Carpenter et ai . I9S1). A similar

listed in California, which had a population of 40 million layer (Ernst et ai , 1985).

lording certain workers the pathogenicitv of M. Synoviae (MS) infection in broiler

s was well documented (Ghazikhaian gi a] . 1973, KJeven ej a] . 1972; Yoder et al ,

it’s economic significance in layers was unknown Numerous chicken flocks were

:ause of questionable results on their serologic tests for Mycoplasma gailisepticum

>icallv a low number of hens in the flocks were positive reactors to the rapid serurn

nd rarely had hemagglutination - inhibition (HI) titters over 1 : 80 Usually no clinical

observed. Isolates of MG eventually were cultured from most of the flocks that

hat type of marginal serologic pattern. Positive plate test reactions to Mycoplasma

VIS) were not usually seen with sera from flocks under study. Attempts to isolate

*.a were usually negative although culturing procedures were not intensive in early

ch terms for the isolates as "variant mycoplasma" or "a typical mycoplasma" infection

jsted (Caraig, 1972; Yoder. 1972; KJeven, 1975). Progeny reared from these involved

ly evidenced clinical disease. During the course of this study, similar reports were

10

J5

Truscotr et al t 1974). Mallinson and Rosenstein i 1976). Mailinson et a], (1981) and

son ( 1981). Tniscott Termed the MG isolates to be or' "low virulence" were MG.

to moderate virulence.

iplasma gallisepticum iMG) infection was diagnosed by detecting specific antibody or

organism from infected birds Although such procedures have been invaluable for

e status of breeding stocks in control programs and for routine diagnosis, it has been

zed that cross reactions and non-specific reactions in serologic tests (KJeven, 1975)

lsiiivny of cultural procedures (Mallinson et aj... 1981) have hampered accurate

bridoma technology which has been used to obtain pure, specific reagents for use in

ignosis where cross-reactions were problematic iBuck et ah. 1982: Thirkill et ah.

aclonal antibodies have been developed for research and diagnosis for a number of

s (Buck et aj.. 1982. Thirkill et ah. 1985).

cpticnemia.

epticaenua was responsible for significant economic losses in aviculture in many pans

. (Gross. 197S). although the mechanism of pathogenicity of strains of E coli that

ally pathogenic to birds was not fully understood lElwell and Shipley. 19S0)

ertchia cob was regarded as a member of the normal bowel flora of mammals and

tme strains were pathogenic due to the acquisition of virulent factors (Elvvell and

0). In birds. E. coli infections caused many clinical manifestations (Gross. 1984). the

>n being airsacculitis. pericarditis, septicaemia, and death (Sojka. 1965)

Cholera (Avian Pasteurellosis).

cholera, caused by Pasteurella multocida. remained a disease of major economic

despite more than 100 years of research (Rhoades and Rjmler. 1985) Before the

.•rnson University (CL ) strain of Pasteurella multocida was discovered, mortality in

to fowl cholera could reach as high as 100° o (Rhoades and Rimler. 1985) The CU

-en widely used as a live vaccine in the turkey and chicken industries for nearly 2C ??

*

!

;\er. recently the industry has become concerned that the live CL' vaccine might be

ca! fowl cholera Thus there has been renewed interest in vaccinating broiler breeder

inactiv ated P multocida v accines since bacterins protect poorly against challenge bv a

strain of Pasteurella multocida (Heddlesron et al . 1972). there has been increased

eiermining the serotyes of P multocida isolates from field outbreaks

cute outbreak of fowl cholera in one-month old chickens was investigated by Yadav

i. Pasteurella gailinamm was isolated in pure culture from the heart blood of two

icks This seems to be the first record of the isolation of P gallinarum in India.

I cholera caused by Pasteurella multocida was also a commonly encountered disease

ai turkey production, with a flock prevalence in Georgia in 19S6 of IS 0°o (Morris

. 19SS) Information was gathered through case and flock records and from telephone

wevs from 45 flock of commercial toms diagnosed with FC at the Poultry Disease

:nter at University of Georgia (PDRC) in I9S6 Birds from turkey growers who

ises to PDRC for necrospy. represent 72 8% of the .1 275. 623 commercial turkeys

iorgia in I9S6 (Morris and Fletcher. ! 9SS ; Strong and Wildey. I9S7) Additional

mation was combined with previously reported findings (Morris and Fletcher. 19S6)

he economic impact of FC in commercial turkeys in Georgia in 1986

literal blood lymphocytes (PBL) from Turkeys immunized against Fowl cholera with a

i live aviruient vaccine (strain CS-I4S) were cultured in vitro with various antigenic

from Pasteurella multocida (Strain P-105g) by Maheswaran et ai (1975). Both

cell medicated immune systems have been shown to be involved in the expression of

a variety of microbial infections (Collin. 1974), Although they were separate immune

v generally interact in complex ways to resist intracellular and extracellular pathogens.

eases, however, one of the systems played the major role in conferring protection

vards understanding immunity to Fowl cholera was impeded by the lack of knowledge

he role of humoral and cellular immunity (TU or CMT) Vaccines that were used in

measures were oil-adiuranted bacterins(g), live aviruient vaccines (Bierer and

72. Maheswaran et af, 1973; Heddleston et al, 1 975),in-vivo-propagated tissue

leddleston and Robers. 1972). and bacterins from infected turkey embryos

i

i!

ia*12

7*

and Robers. 1974) Woolcock ( 1973) believed that cell-mediated immunity played an

e in immunitv to Foul cholera disease

'del-diffusion precipitin test (GDPT1 was considered an accurate, satisfactory method

g strains of Pasteurella multocida (Heddleston et a} . 1972: Blackburn et a]., 1975)

:orts (Blackburn £t a].. 1975: Heddleston and Robers. 1975) have described 15

the basis of difference in heat-stabie antigens Of these 15 serotypes. 7 were isolated

. This note demonstrated an additional serotype recovered from an epornttic of Fowl

examined its pathogenicity in turkeys

ines made from ribosomes of Pasteurella multocida have been shown to protect

gainst fowl cholera (Baba. 1977). Baba (1977) reported that the immunogen

or protection was nbosomal RNA In contrast. Phillips and Rimler (1984) found that

was due to the presence of small amounts of specific lipopolvsaccharide

nts undetectable by most biochemical tests - that contaminated the ribosome vaccine

Although the latter authors found that P. multocida ribosomes were not protective

; for chickens, they showed that ribosomes or their components helped induced

ainst small amounts of LPS These amounts did not induce immunitv when used alone

Aspergillus fumigatus or Brucella abortus ribosomes could replace those from P

> induce immunitv LPS. (Phillips and Rtmler. 1984).

ctious Coryza.

il reports of (Nelson. 1933. Nelson. I93S) on the etiologic agents of Infectious coryza

ignition of the importance of mycoplasma in respiratory disease in chickens

gallinarum (HG) was shown to be a complicating agent in the type III, or

Coryza.

ler ei a], (1977) produced three types of infectious Coryza in unvaccinated chickens by

locuiums containing different combinations of Hemophilus gallinarum (HG) and

a gallisepticum (MG). Monovalent and combination bacterins of the HG and MG were

letermine their efficacy against chroruc complicated Infectious coryza. Challenge

13

f1

t

vaccinates with MG and HG showed protection against the HG component to be

specific Some protection against complicated Coryza resulted from HG bacterins

is Mg bacterin was ineffective protection against transient and chronic Coryza was

a combination MG-HG bacterin Two doses of this bacterin gave better protection

respiratory clinical signs and lowered the incidence of airsacculitis.

dicated Coryza has been reproduced experimentally with Mycoplasma gailisepticum

IG) m combination ( Adler and Yamamoto. 1956. Kato 1965) However, there have

dished repons on this complex disease. The absence of case repons suggested that

Cory za was either relatively rare or that it might had been unrecognized

nv other countries, however, there were indications that the latter might be the case.

Is have been toward returning to multiple-age-poultry operations, should that

nil uncomplicated and complicated Corvza were a potential hazard. These

s were conducted to determine whether complicated Coryza could be prevented or

bv using bacterins against H gallinanam and M gailisepticum.

Typhoid.

tvphoid was worldwide in distribution. The disease has been of considerable

tponance in United States (Hall and Cartnte. 1961. Pomeroy. 1972) especially in

ten outbreaks in chickens and turkeys increased dramatically in number It was

ne of the greatest disease hazards to the poultry industry along the eastern seaboard

972). In 1975. 16 cases were reported in the United States (AAAP disease report

1975) The dramatic drop in fowl typhoid outbreaks was related to the

ihoid control program (Pomeroy. 1972) of the National Poultry Improvement Plan

aboratory tests based on blood samples from sick birds were positive to the

ihoid test. S gallinarum was isolated along with Escherichia coli. Enterobacter Sp ,

.x Sp.. and Staphylococcus aureus .Ail of the birds eventually died front a

of fowl typhoid and neglect. The chickens in both flocks appeared droopy, with

ers. as the mortality began to increase. They did not respond to terramvcin treatment. :

1-5

l

%

;< birds submitted from flock 1 to the diagnostic Laboratory were dehydrated and has

is on the heart and small abscesses in the liver Sick birds submitted from both Hocks

. after mortality started were dehydrated and had mottled greenish-brown swollen

ante peritonitis In flock I mortality reached a peak on the sixth day. on which day

e birds died within 30 days, over 98% of the Hock had died. No mortality record was

k 2

I tvphoid was reported to be a septicemic disease of domesticated birds, The course

ule or chronic and the mortality moderate or very high, depending largely on the

the inciting organism. Salmonella gallinamm (Hall et ah. 1949; Pomeroy. 1972)

on et al (1QT“1 diagnosed Fowl typhoid in a one year old light-breed

aying chicken breeder flock and in a 16-week-old progeny pullet Hock on the same

mella gallinarum was cultured from chickens in both flocks, signs and lesions were

disease was confirmed to the one farm The source was suspected to have been a

aminated well They described an acute Fowl tvphoid outbreaks in a breeder flock and

15

*

\L DISEASES.

Pox.

pox (FPi was reponed as an acme contagious disease caused by FP virus, outbreaks

as affected the poultry industry in many countries (Biggs. 19S2), with infection

ough mechanical transmission by mosquitoes and mites The lesions often developed

mis. the feather follicles, and in some cases the mucosa of the mouth, oesophagus.

;al chambers, larynx, and trachea. In the diphtheritic form, white opaque nodules

mucous membranes, rapidly increasing in size and coalesce to form a yellow caseous

mane (Richter-Reichhelm et a].. I9S5). Infected chickens presented severe respiratory

gin be followed by suffocation Histopathologically. the most important features were

if the epithelium and enlargement of cells associated with inflammatory changes and

: eosinophilic cytoplasmic inclusion bodies (Bollinger bodies)

pox one of the oldest known viral disease of chickens, has been eliminated from

•rcial poultry farms in many pans of the world through use of the attenuated fowl pox

i. Since many Poultry farms have discontinued the use of the vaccine in their flocks a

puble chicken population has consequently been prouded.

Talent Fowl pox virus was isolated from a natural outbreak of the disease in sudan by

1 (1979). The virus was used from experimental transmission of the disease to

chickens Scarification and intravenous methods were used to infect one-month-old

carification induced typical pox lesions at 5-7 days Postinoculation, whereas

injection induced onlv swelling of combs or wattles, at 10-1 1 days postinoculation.

rutralizing antibodies against fowl pox virus were detected 2,3 and 4 weeks

ion. The histopathological features of the pox Lesions obtained in both natural and

! infection were described

I pox virus infects susceptible chickens of all ages. During natural infection, eruption

ns on various pans of the body was suggestive of fowl pox infection. Extension of the

nd the eyes might lead to partial or complete closure of the eyes. In the diphtheritic-

disease. lesions appeared in the mouth, esophagus, and trachea. Infection in young

16

f

ay caused generalized lesions, poor feathering, and death. Egg production of layers

Juced ( Beach. i°29)

athv el ill (1974) made 2 isolations of Fowl pox virus from hens of an aduk laying

.ÿ university of Illionis poultry farm. The birds from which isolations were made had

lesions on the comb and wattle Periodic drops in egg production had been observed.

as virulent for susceptible day-old chicks Since indirect ev idence had indicateda drop

on in naturally infected birds, the effect of this virus on layers needed funhei

n.

Fowl pox virus originally isolated from mild lesions from naturally infected chickens

it to be an avirulenr strain, was highly pathogenic for susceptible day-old chicks

t a]., 1°74) the observations in the study with a limited number of birds showed its

ty for adult birds bv producing typical lesions and causing a drop in egg production

her conditions, e g . nutritional or environmental were associated with the reduced egg

after experimental inoculation with Fowl Pox virus, the infection was believed to be

a drop started from the second week after inoculation and continued until the fifth

imilnr reduction occurred in the controls

ison (1931) also observ ed a marked drop in production in birds following vaccination

attenuated Fowl pox vaccine.

nilder forms of Fowl pox a decline in egg production might not be associated with

ifection when only minor localized lesions occurred. Before the isolation of Fowl pox

iginal affected flock, periodic drops in egg production had been recorded but were not

with Fowl pox infection. Jones and Jordon (1976) reported reduction in egg

in a slowly spread natural Fowl pox infection in unvaccinated birds. While the

esion was involvement of the larynx, with isolated both from the cases of laryngeal

'om scars on the combs.

iathy and Hanson (1977) observed that egg production dropped after hens were

with Fowl Pox virus originally isolated from a natural mild infection. The drop started

id. week and continued to the 5th week after inoculation. All birds developed focal

Ihe sue of inoculation :iml some developed secondary lesions. The drop in individual

related to the severity of lesions Birds challenged with Fowl pox virus fifteen months

ination with pigeon pox vaccine were susceptible Following diagnosis of Fowl pox

n the birds of the poultry farm, vaccination with a pigeon pox vaccine has been done

ii S to in weeks of age and no further clinical cases of Fowl Pox was observed.

and I lanson. I977)

.aga el al ( 1979) observ ed that atypical Fowl pox occurred in several poultry farms in

two occasions layers had t heir eyes closed and egg production dropped Fowl pox virus

ed from lesions on ;be inner surfaces of the closed eyelids. Other chickens bad lesions

v yellow caseous necrotic material in the mouth, around the epiglottis, and in the trachea

tae Typical proliferative cutaneous lesions were observ ed in birds of all ages in other

nnined Fowl pox virus was recovered from both cutaneous and diphtheritic lesions. The

ehoiioallantoie membranes had focal hyperplastic lesions containing pink-staining

ilasmie inclusion bodies in most cells. Transmission studies showed that the virus was

.dent to susceptible chickens

Tedious Bursal Disease (Gmuhoro Disease).

lections bursal disease (IBD) is said to be an acute and highly contagious viral disease of

ickenx that was first described by Cosgrove in 1962. Age appeared to be an important

natural Infectious bursal disease virus (IBDY) infection. Chickens were most susceptible

1 infections from 3 to 6 weeks of age (Ley et al., I9S3), although the disease has been

to occur in 2 to 15 week-old chickens (Ley et a! 1979). Chicks that were susceptible

than 2 weeks of age were subclinically infected, but the infection usually lead to

.ippression (Hirai et a|., 1979). The mechanism of the immunosuppression was not fjlly

id but presumably resulted from the destruction of differentiating lymphocytes (Hirai,

Tedious bursal disease virus (IBDY) the causative agent of Gumboro disease of

that was lirst described by Cosgrove (1962), was a double segmented, double-stranded

IS

is belonging to the Birna vims family (Dobos sil al, 1979). Infectious bursal disease

of great economic significance in file poultry industry', as virulent field viruses could

lighlv contagious immunosuppressive disease that might lies exacerbated infections

other etiologic agents. The disease which has the greatest impact on young chickens,

oduced lesions within the Lymphoidal follicles of the bursa of Fabricius (Fadlv £t al.

: principal methods of controlling 1BD in young chickens were vaccinated with an

1DV strain or transfer of high levels of maternal antibody induced by the administration

killed IBDV v accines to breeder hens (Wyeth and Cullen, 1979).

,‘ctious bursal disease (IBD) is reported as a contagious disease of young chickens

a virus that was tentatively classified as a birna vims (Dobos £1 al-. 1979). The disease

Ifected the bursa of Fabricius and, to a lesser extent, other lymphoid organs (Fadly si

)ohmsetai. 19S 1).

actions bursal disease (IBD) was a lymphocytolvtic disease of chickens. The etiologic

ictious bursa! disease vims (IBDV), was classified within the family Birnaviridae

id Hiichner. 1984). Clinical IBD in fully susceptible 3-to-6-week-old chickens has a

>ation period and acute course characterized by high morbidity and variable mortality

id Hitchner. 1984). In contrast to the clinical disease, subclinical IBD has been

I in susceptible young chickens less than 2 weeks of age (Allan el al., 1972). This form

.ease produced immunosuppressive sequelae that have been studied extensively in

experiments (Lukert and Hitchner. 1984).

ectious bursal disease vims (IBDV) was the causative agent of a highly contagious

young chickens (Gumboro disease) characterized mainly by severe changes in the bursa

is followed by immunosuppression (Allan, £i al , 1972; Hirai el a!., 1974, Fadly £i al ..vas well known that the vims persisted in the environment, and once the infection was

1 on a farm, it reoccurred in subsequent flocks (Edgar and Cho, 1965; Benton gt al,

;ar and Cho. 1973). Pathogenic strains of Infectious bursal disease vims (IBDV) caused

bursal disease (IBD) in chickens characterized by severe damage in the bursa of

ind immunosuppression (Cosgrove, 1962; Cheville £i al.1967; Allan £i al.. 1972). These

re classified as serotype I vaccines (Saif, 19S4), and all the commercial vaccines were

19

this serotype. Report on the isolation of serotype I IBDVs from commercial broilers

•ursal lesions and adequate levels of maternal antibodies against the vims were well

(Saif. 1084; Brown. 1086; Rosenberger and Cloud, 1086; Saiffiiai.. 1087). These

*s were designated as variants, w hereas viruses recovered before 1084 were designated

I or classic viruses. In this report information was presented on the characterization of a

i(from layer pullets) of serotype I 1BDV that was related to the variant strains isolated

;rs.

ectious bursal disease (IBD) is said to be a highly contagious viral disease affecting

hickens throughout the world. Some of the clinical signs in chickens first described by

(1062) included whitish or watery diarrhea, anorexia, trembling, and prostration

n young chicks could result in immunosuppression (Allan el a|., 1072; Giambrone et

>. The primary target organ of IBD vims (IBDV) is the bursa of Fabricius, although

damage might occur in the spleen, thymus and gland of Harder as well (Cheville, 1967;

Q!.. IOSI)

e chicken is considered the principal species in which natural IBDV infection occurred

here have been reports of IBDV isolation from turkeys and ducks (McFerran. e; a] ,

contrast, Japanese quails were reported to be refractory to IBDV infection; they tested

ir vims reisolation, detection of precipitation or vims neutralizing antibodies, and both

ind microscopic changes in the bursa of Fabricius associated with infection (Weisman

ler, 1078)

ectious bursal disease vims (IBDV) has been classified into two serotypes (Jackwood el

An IBDV isolate from chickens, two commercial IBDV vaccine viruses and the North

1C) strain (a turkey isolate) have been designated Serotype I; two IBDV isolates from

lie Missouri (MO) and Ohio (OH) strains-have been designated serotype II (Jackwood

’).

ickens were chemically bursectomized by Fadly el af (1976) with cyclophosphamide at

. and studies made of the effects of infection by inclusion body hepatitis vims (IBHV)

oils bursal disease vims. In another experiment, 3-week old chick were infected with

bursal disease virus before inoculation with IBHV. interference with the bursa of

20

i:ii

iv cyclophosphamide or by Infectious bursal disease virus enhanced the pathogenicity o!'

contrast, cyclophosphamide effects on thebursa protected chickens against Infectious

;ase.

of the clear delineation between thymic and bursal lymphoid tissue in chickens,

m of normal bursal development with result in severe defects in the ontogeny of

mnume response (Payne, 1971 and Hammer. 1974), Bursectomv has been used to

with bursal development such bursectomv can be accomplished surgically, by

ing hormones, or by total-body X-irradiation (Payne, 1971). Lerman and Weidanz

.o showed that cyclophosphamide (CY) (Kaplan and Calabresi. 197.1) interfered with ;he

of the humoral immune response in chickens - CY has been used also as a humoral

ippressant. in immuno-competentinice. to study the immunopathogenesis of lymphocytic

tingstis (Gilden. 1972). Willenborg el a!. ( 1971) found that genetically resistant CH mice

iered susceplible to mouse hepatitis virus by treatment with CY.

te role of humoral immunity in disease resistance has been investigated by studying the

of hursectomized birds to various infection. In 1959, chang £1 al- ( 1959) demonstrated

sectomized chickens were far less resistant to Salmonellae lyphimurium than

omized control birds. Baluda (1967) found that hormonal bursectomy interfered with

:ent of normal resistance to avian myeloblastosis virus. Peterson el af (1964) and

Si ill (1966) indicated that surgical bursectomy during the first month of life protected

from Lymphoid Leukosis. Bursectomized chickens were more responsive to avian

myelitis than were normal control birds (Cheville, 1970). and challey (1962) observed

I rates from Eimeria tenella were higher among bursectomized birds. No work has been

scribing; the role of humoral mediated immunity in the pathogenicity of inclusion body

virus (IBHV). Wintcrfield el af ( 1973) indicated the difficulty of reproducing inclusion

>ntitis (1BH) experimentally in chicks older than 10 days. Most field cases of IBH,

occur at 5-9 weeks of age.

was apparent that impairment of the bursa of Fabricius (by CY or bv Infectious bursal

irus) rendered chickens vulnerable to IBHV infection, others (Lerman and Weidanz.

ve shown CY to have no effect on thvmic-dependeni immune function in chickens It was

21

‘

J

(he biological protection against IBHV was chietlv mediated through antibody forming

v The dilliculty of producing IBH in SPF chickens older than 10 days (VVinterfiled el

revealed (hat field cases of IBH might be preceded bv a stress on the humoral immune

It was obvious from these studies that Infectious bursal disease virus enhanced the

:ity of IBHV. Because Infectious bursal disease and IBH were both diseases of young

t was suggested that the immune status of a certain Hock to infectious bursal disease

Ally affect the incidence of IBH upon exposure to IBHV. Similarly, lack of immunity to

bursal disease virus in breeder flocks was recently related to an increased susceptibility

/ to hemorrhagic aplastic-aneniiasyndromc and gangrenous dermatitis (Rosenberger et

that was relevant since Infectious bursal disease virus has been shown to be a viral

ppressant agent for chickens (Favagher et a].. 1974) Protection of chickens against

bursal disease by CY treatment was similar to their protection from Lymphoid leukosis

I bursectomy (Peterson et al . 1964: Peterson el ah. 1966) This indicated that normal

s must be present for Infectious bursal disease virus to induce clinical signs and lesions

ease Infectious bursal disease and Spirochetosis were diagnosed simultaneously in a

00 six-\veek*old babcock pullet chicks. Larvae of the fowl tick Argas persicus were

he bodies of the chicks. Thirty nine of the chicks died 5 days after the onset of clinical

e differences between species in susceptibility to IBDV infection provided an

:y to examine the genetic factors involved in susceptibility. The quail-chicken hybrid has

j| in studies of genetic regulation of isozyme expression and activation (Levine and

775), genetic interactions of blood proteins (Lucotte el al., 1978), and on

‘mental cell-structure glycoproteins (Dietert ela].. I9S4).

'ectious bursal disease vims (IBDV) replicated in lymphoid cells of the bursa (Hirai and

979; Muller, 1986) and induced atrophy of this organ as a result of necrosis of

tes. The availability oflarge numbers of bursal cells (B cells) has been shown to be an

actor in the development of IBD (Ismail gial., I9S7).

interfiled el al. ( 1972) reported that Infectious bursal disease vims (IBDV) affected the

•abricius of young chickens, and produced a variety of syndromes ranging from loss of

22

*

mcy and to ablation of the humoral immune response. Control of Infectious bursal

oved difficult lor at least two reasons. First, because of the common occurrence of

infection (Lukert and Hilchner. 1984), the disease often went undiagnosed, because

ve vims vaccines were commonly issued in young birds (Winterfiled el a!., 1972), and

icy for these vaccines depended on successful replication within the birds, assays for

f field-origin virus could be confounded by the presence of vaccine viruses.

iller, 1979 classified IBDY as a birna virus. Its biseymented double-stranded (dsRNA)

1979) was contained within a 60 - nm nonenveloped capsid. Electrophoretic

ns to RNA standards under native and denaturing conditions have revealed the two

zes to be about 3400 and 2900 base pairs (Azad ei ah, I9S5).

:thods for detection and quantitation of antibody levels against Infectious bursal disease

>V) included tiie virus neutralization (VN) test, the agar gel precipitins (AGP) test, and

e linked immunosorbent assay (ELISA) (Marquardt ei a]., 1980; Snyder el al., 1984;

el aJ - 1985) IBDV serotypes I and 2 could be easily riillerentiated using the YN test

, differences between strains within a serotype could be detected by the test (McFerran

0; Jackwood ei a]., I9S5; Jackwood and Saif, 1987). The ELISA has been used to

measure antigens and antibodies in birds. It has proven efficacious for the quantitation

y to IBDV and for monitoring the immune status in large flocks (Marquardt ei al.,

•erranet ai., I9S0).

4-week-old broiler chicks were inoculated by Jhala, el fli (1990). with Infectious

•ase virus and 6 infected chicks were used as a control. Three birds from each group

j after 48 hours and the reminder after 5 days. No clinical symptoms were observed in

rds, but the agar-gel diffusion test on bursal homogenates confirmed infection after 48

i bursa fabricius (BF) of infected birds was enlarged due to oedema after 4S hours but

after 5 days After 4S hours the BF showed severe infiltration of heterophils, necrosis

irv lymphocytes and hyperplasia of the corticomedullary epithelium. Bursal lesions

were after 5 days, lymphocytes were depleted and fibrous connective tissue had

d. Mild depletion of lymphoid follicles in the caecal tonsils was observed after 48 hours

;. The thymus, spleen and kidneys exhibited no histopathological lesions. Joseph (1990)

23

! J

n*

that sudden high mortality in various poultry flocks in Dominica in April, 1900 was

J as due to Infectious bursa! disease with inclusion body hepatitis.

ifectious bursal disease was diagnosed by Elmubarak, and Abuelgasim, (1990) in May,

the first time in Khartoum area where the highest concentration of commercial poultry

>n in the Sudan was located. During a !2 months period 7 flocks of light breeds were

The age of 5 of the affected flocks ranged between 6-7 weeks and 2 flocks were 12

d. The mortality rate ranged from 0.9-22,7%. Typical symptoms, post-mortem lesions

pathological changes were detected in all flocks. Serum samples contained precipitin

> when tested with known IBD antigen. Vaccination against the disease was introduced

rst time in the country following the outbreak. Imported chickens were the suspected

uring a routine pre-slaughter health examination of 4 1 -day-old broiler chickens, bursal

iridiosis was diagnosed by Bows (1990) histologically. Numerous pale-stairing

iridium sp. w'ere present lining the superficial bursal mucosa The underlying epithelium

derately hyperplastic with an increased number of heterophils present. No

iridium sp. was present in sections of intestinal tract examined. There was no history’ of

sease in this flock during the growing period. Birds had been water vaccinated at day 14

ifectious bursal disease. According to the Rao et af (1990) in a flock of 2500.

old white Leghorns an outbreak of infectious bursal disease affected about 80% of the

rtality was 20%. The clinical sings and pathological features reported were similar to

:ribed previously except that changes in the proventriculus (oedema, hemorrhage) were

this outbreak.

flock of 1200 ducklings 10 days of age at the New Valley duck farm showed sings of

l and diarrhoea with a 50% morbidity rate and 2% mortality rate within a week. I’M

jn revealed severe nephritis and swelling of the bursa of fabricius. Infectious bursal

irus was isolated from diseased ducklings and identified as serotype I by serum

don test (Abdul-Motelib, £t a]., 1991). Serum samples were collected from 7 industrial

>cks and examined for antibodies to Infectious Bursal Disease virus by gel precipitation

logenates of the bursa of 51 birds that died during suspected outbreaks of the disease

24

%

tested. Antibodies to the virus were found in nil the flocks examined, with 1 18 (33.9%)

samples taken being positive. The viral antigen was detected in 9 (29%) of the bursa

he flocks had not been vaccinated against the disease and these observations confirmed

ce of the virus in Cameroon, where mortality rates of up to 25% from undefined disease

eported in previous years.

rita £i ai., ( 1991) studied the pathogenicity of avian nephritis virus (ANV) in 7-day-old

viouslv infected with Infectious Bursal Disease virus (1BDV) at 1 day of age. Of 20

JV-infected chicks, 3 were found dead with no apparent clinical signs within 10 days of

I with ANV and they had marked urate deposits throughout the body. All of the

IBDV+ANV-infected chicks had reduced body weight gain, unlike the ANV-onlv

BDY-only infected and non-infected control chicks In a chronological study, all of the

cted chicks had interstitial nephritis accompanied by tubular cell degeneration and

cell infiltration Avian nephritis virus antigen was detected with equal sensitivity by

t antibody and immunoperoxidase techniques and was widely distributed in the

:d epithelial cells. The concentration of serum uric acid in IBDV+ANV infected chicks

•r than that in ANV-only infected chicks. The antibody against ANV in ANV-ovily

licks was first detected 8 days after inoculation and its titre increased gradually. In the

he antibody in the IBDV+ANV infected chicks w'as very low and was detected in only 3

;hicks 16 days after inoculation; the titre was 1:4 in one chick and 1:8 in the other 2

>incident with the serological results, the number of lgG- and IgM-containing cells in

vs and spleen were less in IBDV+ANV-infected chicks than in ANV-only infected

hese findings suggested that IBDV infection in chicks might influenced the

gical response and susceptibility to subsequent ANV infection.

rg el af. (1991) isolated a highly virulent strain of Infectious bursal disease virus

om the field and propagated in SPF chickens, causing up to 100% mortality. Although

onged to the standard serotype l-IBD viruses, serological typing with monoclonal

showed an antigenic drift in this pathogenic strain. Conventional "intermediate" IBD

re probably more antigenically related to the pathogenic strain than the mild ones and

tive in protecting SPF chickens against challenge.

25 1

ifiVi

.1

inphoid Leukosis.

jghes el iH. (1063) reported the development in one generation of a small experimental

lock apparently free of LLV by pretesting a series of embryos from selected

positive dams. The relatively cumbersome test procedures available at that time,

precluded attempts on a commercial scale

.ms from a commercial source were selected by Spencer si Q\. (1977) because they were

vith Lymphoid Leukosis virus (LLV). LLV was detected in vaginal Swabs from 17

;ns and from 27 of 44 hens that were not viremic All hens that were positive on the

vab test (VST) produced one or more eggs with virus in albumen or in embryos.

i comparable tests, virus was detected only in eggs from 5 of 17 hens that were negative

Congenital transmission of LLV was erratic and neither the VST nor tests for virus in

ten prior to incubating eggs identified all hens that transmitted infection For example.

iegative on VST produced 50 eggs negative for virus in albumen and yet one of the

rom these eggs was infected. Eggs from other hens had infectious virus in albumen and

f of the embryos from these were infected. Tests for virus in cloacal swabs from

Id chicks were as sensitive as tests on embryos for detecting congenital transmission.

„LV in the meconium of congenitally infected chicks were as high as 107 infectious unit

le authors suggested that cloacal swab test should be a valuable adjunct to the VST and

ig albumen in programs designed to eradicate Lymphoid Leukosis from chickens.

mphoid leukosis in chickens was a malignancy of lymphoid tissue dependent on the

:abricius. While mortality from this disease occurred only sporadically in most poultry

bclinical infections with the causative virus were widespread and probably occur in all

al poultry tlocks (Purchase and Burrnester, 1972) The infection spreads congenitally

to progeny or horizontally from chicken to chicken in the same flock. Studies by Rubin

iates (Rubin el a!., 1961; Rubin et aj., 1962) showed that congenitally infected chickens

tunologically tolerant in that they failed to develop antibody and were permanently

hey determined also, that a high percentage of progeny from immunologically tolerant

congenitally infected In contrast, chickens infected by horizontal transmission usually

antibody, and congenital transmission from such hens was often highly erratic. With the

I26

5

developed hv (Rubin el a]., I960, Rubin el id.. 1961, Rubin el al.. I%2) it has been

to develop Hocks of chickens free of infection with LL viruses (LLV) (Hughes el .if,

nder el af, 1975) Since, however, identifying hens that transmited infection erratically

001. C'alnek, 1965) was diHicull. the disease has been eradicated only from Hocks used

r experimental purposes.

he chances of identifying hens that were erratic in congenital transmission of infection

greatlv increased by the discovery that eggs might contained infectious virus in albumen

ncubation even though embryos which developed subsequently in the same eggs might be

for virus Even so. not all liens that transmit infection could be detected by testing for

albumen because infected embryos had been obtained from eggs that did not have

s virus in albumen (Spencer el al . 1976). In light of these findings it was necessary to

sh between congenital transmission and shedding of virus. The term congenital

lion was used here to indicate infection of the embryo with vims derived from the dam.

Shedding of virus refered to the release of virus from cells of the dam into the egg

In addition to shedding virus, some hens also shed group-specific (gs) antigen into egg

The gs antigen was considered to an internal structural component of the vims that was

to viruses of the leukosis sarcoma group (Bauer and Schafer. 1966; Purchase and

;r, 1972). The overall objective of these studies was to develop methods that would

the efficiency of programs to eradicate IT. specific objectives were : I) to determine

LLV could be detected in vaginal swabs from viremic hens and from nonviremic hens

:antibody-positive ; 2) to determine interrelations among infection in hens, the presence

or gs antigen in egg albumen, and infection in embryos : and 3) to determine whether

ally infected progeny could be detected by testing for vims in swabs from the cloaca. The

ave application in eradication of LL and gave insight into mechanisms of congenital

»ion.

)kazaki £t al. ( 1979) conducted two trials to determine whether Lymphoid leukosis vims

uld be eradicated from chicken breeder stocks in one generation. Dams were selected as

ly virus free parents on the basis of negative tests for virus in progeny embryos (trial 1)

ginal-cloaca! swabs (VCS) (trial 2) of the dams. In trial l.S of 12 groups of chickens

i27

r

om selected breeders remained free of LLV infection through 30 weeks. In trial 2.YCS

to be more ell'icient in detecting shader dams, and only one of 72 groups of chickens

vidence of infection at 14 weeks after hatching within that positive group a single

as shown to be the positive cause of the infection. The results showed that eradication

ould be accomplished in one generation by . I ) virologtcal examination of dams for

21 elimination of the shader dams : 3) small-group rearing of the progeny chicks.

leukosis viruses (LLV) were found in most commercial poultry tlocks. and

kens in a tlock were exposed to infections, and most virus at some time during their life

.•the: an infected chicken eventually developed lymphoid leukosis (LL) depended on a

'circumstances . age of exposure level of exposure . genetic susceptibility, of the strain

I levels of maternal antibody and other important factors still undefined. Early, several

ors < Burmester etal . 1935; Burmester and Waters 1955; Burmester and Waters, 1956;

id. 1961; Rubin el af, 1962) and Weyl and Dougherty (1977) showed that the major

lansmtssion of L.LY resulting in LL was by congenital infection from dam to Offspring.

Inis congenitally infected were usually immunologically tolerant to LLV usually remain

'i the rest of their Lives, and. in turn, when mature, produce a high frequency of infected

When infected by contact or horizontally, chickens developed transient low-level

with subsequent development of neutralizing antibodies that persisted for long periods,

iced infected progeny inconsistently.

I

:

i

wider el al. ( 1975) reported the establishment of 3 breeding lines of chickens free of LL

IK hiding a white leghorn Layer, brown - egg layer, and a broiler line. The virus detection

wis the resistance - inducing factor (RJF) test. In the white leghorn line, RJF testing and

through 4 generations was required before the birds were free of virus. The relatively

velopinent of more economical and rapid test procedures (Spencer et al . 1976) suitable

g larger numbers of samples has opened the way to an evaluation of testing protocol for

ig LLV in commercial flocks. The objective was to evaluate these new test procedures

mine whether LLV could be eradicated from commercial chickens in one generation.

pencer el ai (1976) found high concentrations of LLV group specific (gs) antigen in

of chicken eggs and high concentrations of LLV in most of these (gs) antigens were:

28

rin some albumen samples, however, although low-levels of virus (102 to 104/ml) were

bv the viable-virus-assay phenotypic mixing of tests (PM) : gs antigen concentrations

amiably below detectable levels Many years ago Burmester (1956) and Burmester and

1054) reported the shedding of LLV in feces and saliva, and. more recently Weyl and

y (1977) have reported quantitative rates of shedding. They found very high

tlion of LLV in feces and saliva as well as in cloacal swabs from congenitally tolerant

mis, and lower concentrations in the same materials from birds that were contact-infected

hing.

vian Leukosis viruses (ALVS) could be congenitally transmitted in exogenously infected

onsequentlv, progeny immunologically tolerant to ALV recycle viruses of subgroups

id D to succeeding generations (Purchase and Payne. 1984), genetically related, but

igenic endogenous ALV. Which was classified in subgroup E. and was transmitted

he germline and expressed as Mendelian genes.

larek’s Disease.

larek’s disease (MD) is said to be a highly contagious neoplastic disease of domestic

caused by a herpesvirus (MDV). The pathological changes of MD were characterized by

la formation in the viscera and lesions in the peripheral nerves. It was well known that

fection persists over a long period and that some infected chickens actually developed

VID. Some investigations proved that the incidence of MD was correlated with virus

ation in chickens at the initial stage after infection and also with persistence of infection

ilal, 1971; Biggs el al., 1972; Steck and Habarstich, 1976; Fabricant £l a!., 1977). Since

: of the poultry industry has been increasing, the use of a reliable vaccine to prevent

;s of MD in poultry farms was very important. The turkey herpesvirus (HVT) vaccine has

wed to be highly effective in reducing the mortality of chickens from MD (Okazaki £1al,

irehase et si., 1972). However, MD was still one of the major causes of poultry losses in

countries of the world, even in the presence of vaccine (Okazakiet al, 1973; Cho e; af.

dsonfilsl., 1981).

1

29

r

'oinentionally. natural resistance to MD has been viewed as being of two types : "genetic

e", in which chickens were resistant to a virus challenge at I day old (Asmundson and

32; Cole 1968. Crittenden el a!., 1972), and "age resistance", in which resistance was not

d to an early challenge; but was developed with age. The use of the terms "genetic

e" and "age resistance" has implied that resistance at two age levels might be distinctive

:ter. Some authors observed (Sharma and Stone. 1972; Sharma, 1973) that chickens of

genetically selected for resistance to MD) inoculated with MDV at hatching either

:d no detectable lesions of MD or developed lesions only in very low incidence. Because

sistance, older (resistant) chickens developed lesions that were overcome (Sharma et af,

appeared that lesion regression in age resistance and lack of lesion developed in genetic

e might serve as a base for distinction between the two serve as a basis for distinction

the two types of resistance. However, earlier studies were complicated by the presence

nal antibody (Mab) in experimental chickens at the time of vims exposure. Mab has been

.ÿ> provide substantial protection against MD (Chubb and Churchill. 1969; Ball et af. 1971,

1972. Spencer and Robertson. 1972) and it was likely that lesion induction in Line-6

. may have been kept at a low level by the protective effect of this antibody (Calnek,

There have been several isolations of apathogenic strains of Marek's disease herpesvirus

) (Biggs and Milne, 1972; Cho and Kenzy, 1972; Rispens el a!., 1972; Smith and Calnek,

3esides the lack of pathogenicity, little has been known about the invitro biological

es of the apathogenic MDHV as compared with those of the pathogenic MDHV, except

e observations on plague difference between them (Biggs and Milne, 1972, Cho and

1972; Rispens etal-, 1972).

n 1972, Payne and Rennie (1972) reviewed the pathogenesis of Marek's disease (MD)

med unpublished observations, later detailed (Payne el af, 1976), forming the basis for a

sis which appeared fundamentally correct. Briefly, he and Rennie found that neonatal

omy. coupled with subletha! X - irradiation, increased the incidence of lymphomas in

lly resistant chickens subsequently exposed to Marek's disease vims (MDV) but had the

; effect with genetically susceptible chicks. They concluded that the thymus was the

>f the neoplastically transformed cells composing one component of MD Lymphomas and

30

rhe thvnuis - dependent immune system was significant in surveillance and control of

irma ( 1075) Selected chickens of line 6 and N for resistance to Marek's disease (MD)

g maternal antibody, were resistent to MD mortality when exposed to pathogenic MD

)Y) at 1 day old. This finding indicated that natural resistance to MD was well

at hatching in certain lines and was not dependent upon increasing age. Evidence

or lesion regression in early resistance and for possible genetic control of resistance

vith age indicated that resistance at hatching and at that acquired with age might be

character and might represent early and late manifestations of common natural

possible mediated through similar mechanisms. Marek's disease virus (MDY) is a

ated herpesvirus that causes a neoplastic disease in chickens. MD is characterized by

cell proliferation, which in susceptible chickens is usually quite extensive and may be

ne chickens, however, are naturally resistent to clinical effects of MDY The

sties of this natural resistance and the mechanisms through which it is mediated have

considerable interest in recent years.

hen three pathogenic and four apathogenic isolants of Marek's disease herpesvirus

were compared, the pathogenic isolants differed from the apathogenic isolants in their in

vth and sensitivity to plaque inhibition by dextran sulfate.

aques by the pathogenic MDHV isolants were distinctively different in their morphology

e by the apathogenic isolants. the plaque difference being and most pronounced in chick

broblast (CEF) and duck embryo fibroblast (DEF) cell cultures. The pathogenic isolants

laques similarly in both CEF and DEF than in CEF cultures. The sensitivity to plague

by dextran sulfate was greater for the apathogenic isolants than for the pathogenic

f MDHV (Cho, 1975).

ilnek el a], (1977) studied to learn whether "low virulence" isolants of Marek's disease

JS have a low inherent oncogenic potential. 3 isolants (CU-l, CU-2, S-l 1) were given to

y susceptible S-strain or P-line birds with or without immunosuppressive treatments

l lesion incidence and type during an 8-10 weeks experimental period embryonal

bursectomy and neonatal cyclophosphamide (CY) treatmentwere without effect on

31

;

I

F

! CU-2 infections in P-lines. S-ll virus was virulent for P-line, and CV treatment

,1D incidence as reported by others for virulent virus infections. Neonatal thymectoinv or

in ova (at 8 days of incubation) or use of the more susceptible S.Strain chicks ail

the incidence of MD induced by CU-I and CU-2 viruses. It was concluded that the "low

' of these viruses is a rellection of an adequate immune response by the host

dditional information gathered from several Laboratories made it abundantly clear that

is does indeed have such a dual role in MD. Neoplasticallv transformed cells have been

as T-cells, largely on the basis of studies with lymphoblastoid cell lines (Nazerian et 3]..

nvell ah, 1974, Mutsuda et ah, 1976). Impairment of the thymus - but not

pendent immune system has generally resulted in atleast partial abrogation of the

; they have come to associate wiih immunological competence in chickens (Sharma £t

Sharma and Witter, 1975). Virtual elimination of the thymic cells in a chicken appeared

nate MD tumors as a possible consequence of infection (Sharma, personal

ication). The bursa of Fabricius does not play a central role in the pathogenesis of the

ince bursectomy has neither of those effects (Fernando and Calnek. 1971).

hose studies centered on the virulent strains of MDV have approached the question of

:esi$ by comparing various events in experiments with a single variable, e g., age. genetic

id virus strain (Calnek, 1973; Smith and Calnek, 1974; Higgins and Calnek, 1975;

. el ah, 1977). The similarity of pathogenic events during the first 7 days has been

)le. regardless of the variable. That finding, coupled with the favorable curtailment of

in birds destined to survive, supported the concept that it was the host's immune

that was significant.

he picture was less clear with low-virulence MD viruses. It was well established that

ence (and, possibly, avirulent) strains of MDV occurred naturally (Biggs and Milne,

spens £t ah, 1972; Zander et ah, 1972; Smith and Calnek, 1974). Those were several

explanations for the failure, or low probability, of some isolants to cause neoplasms.

ilt with virus - controlled, host - Controlled, and virus - host interaction events. One of

important and first questions to be answered is : does "low - pathogenicity" virus have

potential, or is low pathogenicity a function of a superior host response?. To

he first part of the question, they studied the effects of low-virulence virus in normal and

32

f

lly compromised chickens, and under condition in which the immune response

:cted to be poor.

tta presented by some workers strongly suggested that Marek's disease (MD) was

i to virus multiplication, especially at an early stage after inleciion(\Vitter £l al .el a!., 1976); Fabricant elal., 1977), and to the persistence of infection. (Witter gt

tter el al., 1971; Johnson et a]., 1975; Steck and Habarstich. 1976) Steck and

976) reported that most chickens succumbing to MD persistentlv possessed

• antigen, whereas the antigen slowly disappeared in infected chickens that remained

hy.

loma in Marek’s disease (MD) occurred in various organs, such as the liver, spleen.

•. and gonads The pathology and pathogenesis of visceral lesions in MD have been

many workers (Sevoian and Chamberlain, 1964; Purchase and Biggs. 1967; Mass £i

chneretaj, 1971; Fujimoto el al , 1971, Ratzgtal, 1 972; Doak et al • 1975. Szeky

973; Vicker et al. 1967). Since MD (MDV) was first isolated from infected

irimental studies of MD have revealed several characteristic of the MD Lymphoma

pic lymphomas could occur as early as 3-4 weeks after infection (Payne and Biggs.

he lymphoma could occur in one or more organs, and the lesion consists of

ymphoid cells, Pyknotic Lymphoid cells referred to as "MD" cells, and activated

s (Wight, 1962; Payne and Biggs, 1967; Fujimoto el al . 1971; Yamamoto el a]..

e Lymphoma was composed mainly of thymus dependent (T) cells, with a minor

bursa-dependent (B) cells (Hudson and Payne, 1973; Rouse elfll., 1973. Payne el

) not all of the T - cells constituting the tumor seem to be malignantly transformed

ause only a small number appear to have tumor-associated surface antigens, and the

- cells present in the tumor may be reactive cells mediated by the host immune

ter et a]., 1975) : (e) although viral antigens and virions in the lymphoma were rare.

could be detected in a majority of cells by in situ nucleic acid hybridization (Ross el

ind (I) some of the microscopic Lymphomatary lesions might regress to more

ones (Payne and Biggs 1967, Sharma £i al., 1973).

uchi el a[. (1986) reported that fourteen test groups consisting of a total of 541 Held

; rearing forms, all of which were vaccinated with turkey herpesvirus at one day old.

33

w

ited for chronological changes in Marek’s disease (MD) associated feather-pulp

and their association with nuclear-inclusion (Nl) formation in the feather-follicle

:E) and with incidence of MD The FPL observed were categorized into R,-type

slymphoid lesion), R.-type (intlammatory lesion consisting of plasma cellular in

ma or collagenosis of the pulp, and germinal - center formation) and T-type

lphoproliferative lesion)

rv test group, the incidence of R,-type lesions was highest at 2-4 weeks of age.

ow incidence of Nl formation in the FFE. The initial Retype lesions were generally

were followed occasionally by R.-type lesions. In each test group, incidence of M

he FFE peakedbetween 9 and 16 weeks of age. The second peak of incidence of

ns coincided with the period of peak Nl formation Subsequent skin samples

the incidences of R-, R.-. and T-type lesions in individual chickens or test groups

elated to the incidence ofNl in (he FFE and to the incidence ofMD.

<copic examination of skin samples obtained by biopsy from MDY - infected

useful for determining the MDV - infection level and MD lesion response in

;kens or Hocks (Moriguchi and Izawa. 1979; Moriguchi £t aj , 1982. Moriguchi £t

is method did not require that birds be killed and it has the following advantages

ity in chicken's could be simply evaluated by quantitative observation of the nuclear

) formation in the feather - follicle epithelium (FFE). because the level of virus

te FFE parallels the level of viremia (Tabbu and Clio. 1982) : (b) tumorous or

; MD-associated lesions were found in the feather pulp (Moriguchi el a].. I9S2)

(FPL) were useful in determining the MD lesion response in chickens : (c) small

s could be obtained repeatedly from the same chickens Under such circumstances, a

ion was documented between chronological changes ofNl formation in the FFE and

incidence of MD in chickens experimentally inoculated with MDV (Moriguchi and

Moriguchi si a]., 1982). Moriguchi et a! ( 19S4) reported the correlation between Nl

he FFE and the incidence ofMD in FIVT - vaccinated field chickens.

eaks of paralytic syndrome affecting chickens aged between 2-8 months were

limbita, -EN; and Maeda (1988) in Morogoro. The syndrome caused mortality rates

%, especially in the younger stock. It was diagnosed as Marek's disease by clinical

34 {

pathology, histopathology and virus isolation via the yolk sac and chorioallantoicembryonated chicken eggs. Most birds examined had both neural and visceral forms

>e. The disease was found in breeds such as NY-line. Rhode Island Red. Ross I, Ross

White Leghorn. Light to massive lymphocytic infiltration was observed in nerves and

ins. Of the 13 suspected cases collected from four dilferent route and chorioallantoic

:kens embryonated eggs.

r and Grewal (1980) reported the occurring of MD between November. 1983 and

9S5, 72 outbreaks of Marek's disease were recorded during examination of 1 1000

ortality ranged from 0,2 to 8.4%

*k's disease was diagnosed by Akakpo et al. (1992) on clinical, histopathological and

ical grounds, for the tirst time in Senegal, in February 1989. in layers imported from

ay-old chicks. An atypical from was seen in White Leghorns, and the classical form in

Rhode Island birds.

castle Disease (Ranikhet).

c the last epornitic of Newcastle disease vims (NDV) of the late 1960s to 1970s. the

persisted in the middle east in endemic form. Periodic isolation and typing of velogenic

have revealed the prevalence of isolates of moderate virulence and the occasional

of highly virulent strains Similar to VLT 68, VAUB 74. and B75 isolated between

975 (Zein, 1974; Singh et al., 1978), This report described the biological properties of

rom Saudi Arabia, SA84. A few months following the isolation of SAS4. a severe

varied Lebanon; an isolate from a broiler flock, SML85. had the major characteristics

it it differed in plaque morphology and virulence

atin el ah (1975) reported that vims strain and age of chicken influenced the

lily of lentogenic strains of Newcastle disease vims (NDV) The ability of Lasota. Bl

and ulster strains to spread from cages of oronasally inoculated chickens to adjacent

;cepiible chickens was assessed by vims isolation, serology and immunity to challenge

it NDV. Although all inoculated chickens were immune to challenge, the immunity of

35

1

jkens ranged from 100% for Lasota and CT strains to 0% for ulster strain The

lity of Bl and V4 strains for chickens I, 4, 8 and 16 weeks old was assessed bv within

:t infection, exposure to air from infected chickens serology and immunity to challenge

it virus were used as criteria. Differences in transmissibility were observed for the

us used, route of exposure, and age of chickens, care must be used in interpreting the

of strain differences until the effect of variables can be minimized bv further

its in design of the test procedure.

dilation against Newcastle disease (ND) with lentogenic strains by individual or mass

; was nearly universal. Mass vaccination was used widely in the broiler industry to limit

andling of chick Hock immunity following vaccination by mass application, however.

variable and lower than that induced by individual vaccination methods, because some

o not become infected at the time of administration or by contact with infected

The factors involved in determining the transmissibility of NDV were poorly

, but this paper records the transmissibility of six lentogenic strains of NDV in 6 to 10

chickens and examined the transmissibility of WO strains in chickens at 1.4.8. and 16

re

lough transmissibility was a most important property of strains of Newcastle disease

factory method of measuring it lias not been developed. In an attempt to find a simple

at could be standardized authors tried a design in which 3 groups of susceptible

v'ere infected by seeder chickens under conditions that favour a different mode of

m to each group. While it was important that differences were found between ages and

; strains tested (since it showed the. design to be potentially useful), the strain

could be considered to be significant until the design was standardized and the results

licated in other laboratories.

e primary difficulty in establishing a test for transmissibility was the existence of many

nd intrinsic factors that were difficult to control and that affected the release, transport

ion of vims (Sinha £i <j].. 1954; Beard and Easterday, 1967,). Age of the chicken was a

undamental determinant. The experiments using V4 and Bl strains demonstrated that

iecame more efficient at transmitting virus with increasing age. Failure to understand

36

!

aused confusion (Andrewes, 1945) Other factors that affect responsiveness were

e, humidity and movement of air. configuration of physical facilities and prior

ig of (lie test birds such as food and water deprivation and even the length of time

ds have been caged together (Spalatin and Hanson, 1974). Line of a strain that was

it ulter the results, ulster-purified lias given different results in the hands than

mal. The failure to achieve significant aerosol spread in expeiiment 2 as compared with

: I, may be the difference in the arrangement of cages. In the first experiment, all cages

ie some level and in the second the age of the influence of variables without becoming

nplicated to methodology and to elaborate in physical facilities.

wcastle disease (ND) outbreaks were still common, even though mass immunization

) was practiced throughout the commercial poultry industry. The effects of ND could

n no symptoms or mild airsacculitis to severe nervous and/or visceral involvement

paralysis and death. Broiler chickens were vaccinated against ND commercialiv bv

utes : drinking water, intraocular, intranasal, intratracheal, and aerosol (Allan et a] .

son et al., 1976; Eidson and Kleven 1976). The age at vaccination and the lev el of

mtibodv greatly influenced the hemagglutination-inhibition (HI) response of broiler

Allan. 1975; Kleven ei a] . 1975; Eidson et a! . 1982). There has been a concern in the

ustry that ND vaccines from commercial manufacture may not be inducing a significant

espouse in the broiler chicken Therefore, the purpose of this study was to compare

s of the ND vaccines of seven major ND vaccine manufactures in the United States.

ines, one of high titer and the other of low, were selector for ev aluation of HI antibody

ind resistance to challenge

.cording to Brugli ei a], (1977), replicate samples of serum from chickens immune to

: disease were titrated to determine the intluence of certain test conditions on

lination-inhibition (HI) titters The test conditions studied were those most likely to very

i laboratory operations. The most marked effect on magnitude of HI titters was

I time of twofold serum dilutions in antigen-saline; the average titer increase after

i of the senim-antigenmixturc for 1 hr at 37"C was log 2 3 (five fold) Two fold

in virus concentration of the antigen saline diluent caused an average titer reduction of

37

(

t

ts in HI titters were only minor with two fold changes in erythrocyte concentration

ind with variations in the period between preparation of the initial 1:10 serum dilution

aline and the subsequent serum dilutions (log2 0.3).

-day-old chickens were transported from Australia to Malaysia and vaccinated

!y with an uninactivated vaccine prepared from avimlent Australian Y-J strain of

disease virus (NDY) The vaccination regimes were as follows group A. once, at 2

group B. once, at 3 weeks old; group C. twice, at 2 and at 3 weeks old. group D.

ict with groups A,B. and C, and D. Group F was unvaccinated controls, challenge was

virulent Ipoh AF 2240-226 strain, administered at 4 weeks old intramuscular!) to 10

each group. The remaining chickens were challenged by contact with the inoculated

oup mortalities following challenge were : A. 1/77, B. 1/34. C. 0/39. D. 0/45. E. 6/43.

0 (Spradbrow el aJ.. 1977).

vcastle disease virus (NDY) has been known to Produce conjunctivitis, blepharitis, and

I lens opacities in chickens infected naturally or experimentally (Clark et a] . 1955.

d Beard, 1972; Kaloh. 1977). It has been proposed, but not established, t hat (lie

is of the ocular and periocular regions were of systems in origin (Clark gi af, 1955;

af. 1959; Pannu and Bankowski, 1962; Bankowski £t al . 1963). virus has been

ed in the aqueous humor of chickens infected with NDY ( Dradiri gi af, 1959. Pannu

wski. 1962; C’heville and Beard, 1972), and some authors have suggested that the vims

: aqueous humor through the ciliary body (Spalalin £t af. 1973). Other avian viral

including avian encephalomyelitis and Marek's disease, have been shown to invade the

systemic spread (Flowers el af, 1958).

.vcastle disease virus (NDV) strains differed in pathogenicity in chickens

Juced clinical conditions that ranged from a severe respiratory, neurologic, or enteric

I death to an asymptomatic infection. Rapid differentiation of virulent and avimlent

imperative in order to rapidly initiate appropriate control measures For a long time.

irulence of isolates has been based on pathotyping procedures that included mean death

nbryos, pathogenicity for chickens, and plaquing characteristics in chicken embryo

(Beard and Hanson, I9S4).

different

38t.

1;

\

et a], ( 1984) reported that the first virulent isolates of Newcastle disease virus (NDY)

d from Morocco showed similar properties. It was suggested that in planning control

was important to know whether these isolates were representative of the strains

loroccan poultry Hocks. In order to determine whether the disease in Morocco was

-ingle strain of vims or whether a number of strains w ere enzootic, more isolates had

tiul viruses had been isolated from different sources In t his report, the characteristics

ent isolates from tracheal swabs taken at Rabat lice poultry market and four isolates

cases were described In addition, the viscerotropic properties of the earlier virulent

e reported

(1986) isolated Newcastle disease virus (NDY) in Morocco and characterized it as

Two isolates were from tracheal swabs taken as a Moroccan live poultry market, and

s were from field cases Infection of S-week-old chickens showed that these isolates

isly characterized Moroccan isolates were of the viscerotropic pathotypc Based on

lin thermostability and the capacity 10 agglutinate equine erythrocytes, the Moroccan

isccrotropic NDY isolates were classified as belonging to alleast three distinct strains

ev (1990) rev iewed the mechanisms involv ed in t he spread of Newcastle disease and

mechanisms applied in Australia. Emphasis was placed on the role of wild birds

d partially cooked poultry, windburn spread and human infection. Other aspects

•re the potential role played by game birds, movement of liv e birds, eggs, hatching eggs

d chicks, the role of Hies (Newcastle disease vims has been isolated from Fannia

F. femoralis. Musca domestica), ectoparasites (Ornithonyssus sylviamm. Dermanvssus

id Argas persicus). endoparasites (Ascaridia galli. Eimeria tenella. E. necatrix. E

. rodents, and risks associated with frozen poultry meat and offal

ssell el a|. (1990) studied the antigenic and structural variation of Newcastle disease

monoclonal antibodies and sequencing data were reviewed. It was concluded that no

:rs for virulence had been obtained and the cleavability of the fusion protein remained

mown restrictive element.

•ven Newcastle disease virus (NDV) isolates obtained from outbreaks of disease in

rid Japanese quail in Tamil Nadu. India were characterized by Kuinanan el a!., (1992) in ,

39I

f

:y tests, antigenically, using mouse monoclonal antibodies (MAbs), ' and other

tests devised to distinguish between different strains. All I I isolates were shown to be

ent for chickens. In indirect immunoperoxidase tests used, to assess the ability of a

MAbs to bind to infected cell cultures, 10 of the isolates showed and identical reaction

other isolate failed to react with one MAb which bound to cells infected with the

as Isolate 0 was unstable at pH, while the other 10 were stable. All other properties

I by the I I isolates.

;ara Disease (Hydropericardimn Syndrome).

clinical, hematological, biochemical and pathological changes observed by Jantoso\ic

I) in 5 outbreaks of the disease were described Unsuccessful attempts were made to

lie disease in groups of 10 chicks bv adding cooking salt to the feed of 7-week-old

-10% for a week or furazolidone at 0 08-0 2% for 15 days, one bird in tiie salt group

wlropericarditis.

studv was carried out by Afzal el a! (1991) to determine the etiological agent(s)

with Hydropericardium (Angara Disease) in broilers in Pakistan. The results indicated

ition to adenovirus some oilier agent was involved in causing the disease but that this

ired co-infection by an adenovirus for t he reproduction of the tvpical signs of the

The nature of this agent remained unknown because no discrete virus or virus-like

ild be seen by electron microscopy.

40

VSITIC DISEASES.

diosis.

al Coccidiosis has now been recognized as a problem associated which growing

s of birds in limited areas. Confinement permits the rapid accumulation of the large

locvsts required to produce clinical Coccidiosis. Harmless subclinical Coccidiosis is

le rule in small back yard or rangemanaged flocks. A few omnipresent oocysts may

enelicial in stimulating a gradual buildup of protective immunity. The literature of

imarized in the following paragraphs:

te et a], ( 1976) reported that coccidial life-cycle stages were detected in the bursa of

broiler chickens inoculated with Einteria tenella. whether or not the chicken had

ecn infected with Infectious Bursal Disease vims (1BDV). It was further observed

s infected only with E. tenella had developing parasites in the living epithelium.

.kens with both infections had gametocytes also in the epithelial cells surrounding

generating bursal cysts

(1989) reported the interactions of avian Coccidiosis with other diseases caused b\

uses and mycotoxins. in his review report. The main discussion topics were the

of Eimeria spp. with Marek's Disease vims, reoviruses: Escherichia coli; Salmonella

; Clostridium perfringens He also discussed the effects of Coccidiosis and the

ate of the bird.

(1990) reported that fifty years ago, Coccidiosis was probably the most feared

Ivanced poultry producers of that day. Because of the discovery and use of prev entiv e

iv. that fear is no longer all consuming. However, improving methods for controlling

:oan parasites remains high on Priority lists requesting new research from the poultry

vere mortality losses have become less frequent, but decreased production efficiency

• produce morbidity losses due to coccidial infections. The industry has found that use

:>ccidial drug is generally cost-effective as insurance against losses. However, the

penditure for need of medication in large scale broiler production reminded producers

41

<

ot'this disease would be a continuing expense unless some cheaper method of control

red.

prevalence of parasitic infections in backyard Hocks was surveyed by Nonaka ej

sing litter samples from 74 pens located on 12 farms in central lower Michigan Eight

birds were represented. Two methods of litter examination (a sucrose notation

iiul a multiple washing/ZnC 12 Hotation) were compared during the survey The

arasitc eggs/oocysts were observed, asenrid-type eggs (in .'4 pons from 0 farms).

ggs (in .'0 pens from 9 farms). Strongvloides eggs (in 9 pens from 5 farms). Syngamus

ens from 4 farms), and coccidial oocysts (in 40 pens from 10 farms) Contamination of

ascarid-tvpe eggs. Capillaria eggs, and coccidial oocysts was commonly found.

of bird species. The contamination level in pens with more than one bird species was

in pens with a single species. The relatively high contamination rate may be an

>f the risk of parasitic disease in birds that are not raised under controlled conditions in

t.

patterns of oocyst production of S inbred lines of chickens was compared by

ind Millard. (1992), for each of the 7 species of Eimeria which infected this host Both

numbers and the pattern of oocyst production ditTered in the inbred lines, but there was

:e of prolonged cycling of prolonged cycling of schizogenic developmental stages

n of the numbers of oocysts produced by the different lines indicated that there may be

enctic factors aflecting susceptibility to h of the 7 species. Surprisingly there appeared

iverse relationship between susceptibility to E. tenella and susceptibility to the other

tes which produced most oocysts of E. tenella produced least oocysts of the other

I vice-versa.

42

I

CHAPTER - Ilf

MATERIALS AND METHODS

crimental Material

diseased birds were brought from different commercial poultry farms and the

ere based on the antimortem and postmortem examination of various diseases like

ral and parasitic in various diagnostic laboratories of five districts. The slides and

; of various affected organs and lesions were recorded Following the postmortem

, serologic tests were performed for the differential diagnosis and confirmation of the

hese laboratories.

ce of Data.

data on the poultry birds diseases were collected from the official record of the

:ase diagnostic laboratories of Karachi, Hyderabad. Nawabshah, Mirpurkhas and

e data included observation date, (lock size, morbidity per Hock, mortality per flock,

of disease and the disease name. The data were collected through a survey of the

s.

mortem Examination.

nortem examination was conducted on scientific lines to find out the cause of death

;cord of all the post mortem findings were made during examination and photographs

tern lesions were taken and recorded and detailed history of the farms was also

the proforma specially designed in the form of questionnaire.

43

<

:ase if the bird was alive it was killed by having it’s neck pulled The birds legs were

hand. Grasped the head with right hand so that it rested in the hollow of the hand

joining of the thumb and fore finger. The head was stretched downward direction The

it in a closed container.

thersofthe birds were dis-infected. Bird was laid on it's back legs were separated from

'lie skin was striped back over the breast muscles, sternum and crop Hemorrhages in

md thigh were noted.

ast muscles were looked for tumors. With the help of knife transverse cut at the point

lone was made, with the help of scissors abdominal muscles and the ribs at the

dra! on both sides of the body were cut through and caracoids were cut with bone

vo bronchi and trachea were opened. Underlying organs: breast. lungs, liver, gizzard.

caeca and pancreas were opened by complete removal of breast, gizzard was raised

he entire length of the digestiv e tract was opened lor examination The type of food in

rid gizzard was noted. The proventriculus was examined for thickening in Marek's

for petechialion in Newcastle disease

stines were opened for coccidiosis and presence of worms and were examined for the

langes of intestinal wall and mucosa. Changes in the spleen and liver w ere examined

aries, kidneys and ureters were exposed. The presence of tropical lluid. blood and

il in the abdominal cavity was checked. Nasal sinuses, trachea, air-sacs, bronchi and

examined. The thin triangular shaped muscle that lies on the inner muscle of the thigh

irder to locate sciatic nerve. This nerve nms parallel to the muscle. The brachial nerves

d close to the junction of the wing and body They vverc exposed by removing trachea.

' oesophagus.

loved the skull with sharp scissors and brain was exposed and cerebellum was

>r congestion and hemorrhages.

samples thus found positive in postmortem lesions for any bacterial, viral and parasitic

:. were further processed for serological and other laboratory tests, described below.

at ion of the diseases.

44

r

id Whole Blood Agglutination Test.

test was utilized for detecting antibodies of Mycoplasmosis to find out carriers

carriers under 40-days of age are not positive in agglutination lest, it could not be

: diagnosis of these ages. (Usually the test was performed when they were about

)

requirements and apparatuses used

Diagnostic antigen for Mycoplasma galliseplicum (Mg)

kept it at the temperature of 5C.

Test glass plate 5 to 4 pieces.

Syringe for tuberculin (Icc. injection needle).

Stirring bar.

Stop watch. Record sheets

Alcoholized cotton

Physiological saline solution (0.85%)

The number of chicks to be tested were .500-500 per day

For Mycoplasma galliseplicum 10% per Hock were tested

0 1-02 cc blood was collected from the median wing vein with tuberculin syringe.

On collection, the median wing vein was disinfected by alcoholed cotton

Before and during use, diagnostic antigen was made even by shaking sometimes.

.ÿplasma gallisepticum (Mg)

diagnostic antigen

Whole blood

0.06 cc. (two drops).

(one drop).0.05 cc,

tion temperature 20 C - 25 C.

ement for Mycoplasma gallisepticum

mixing diagnostic antigen with whole blood and stirring

n the sample agglutinated within I minute and become purple

Positive (+).

n the sample agglutinated within I to 2 minutes

-......—> suspicious positive (+ - ).

.ties

45

p

i the sample did not agglutinate after 2 minutes

-...............•• negative ( - ).

! Scrum Agglutination Test.

Plate Method.

itity of the collecting blood

blood was collected front the median wing vein with 5 cc. injection syringe

ration of the Serum.

tlood collected was pm in a test-tube and let to stand until agglutination started and

was let to stand at 20 -?0 C for -I to 5 hours until serum separated

t rapid serum separation was necessary, the blood was let to stand for 1-2 hours and

illigated.

:erum to be used in the agglutination test was not frozen

ug Method.

>plasnia gallisepticum : diagnostic antigen

Serum

0 0.» cc. (one drop)

O.O.i cc. (one drop)

;enicnt.

ement w'as carried out according to the method for the Rapid whole blood

itination test.

•Gel Precipitation for iVlarek's Disease.

position of the Stock Solution of Phosphate Buffer Solution.

jm chloride (Nacl) SO Og

phate chloride (Kcl) 2.0 g

phosphate (Na, H: P04) II.Ogjm

46

ium phosphate (KH, P04) 20g

illed water 800.0 ml

dorm 2.0 ml

ock solution was diluted to 10-folds on using. (1:0)

tsition of Agar Ciel.

ii Chloride S 0 g

anulnr agar l Og

lO-lbld dilution of the stock Sol ) 0 1 0 ml

tlcllind.

ation of Bed

agar gel prepared as described above was put in a dish ((>0 mm diameter)

kept horizontally to solidify

were made (5 mm diameter with 10 mm space).

II amount of agar gel was put in the holes.

lure of Determination of Titer of Antibody.

itigen was put in the central hole.

luted serum was put in the other holes

ved after 24,48 and 72 hours (kept at 37"C).

the precipitation lines appeared between the antigen and the subject serum. MD

dy was judged positive (+) and the final dilution ratio was determined to be the titer

body.

Jure of Determination of only presence of antibody.

ibject antigen was put in the central hole.

47

ibject serum was put in the other holes.

it J7”C and observed al’ler 2d. dS and 72 hours.

the precipitation lines appeared between the antigen

dy was judged positive {+)

and the subject serum. MD

ilass Method.

at ion of Bed.

a slide glass with agar gel. Kept it horizontally to solidify Made holes (7 mm

er with 10 mm space).

lure.

:d similar to that of the dish method

'gliitiiuition - Inhibition Test (HI Test).

st was carried out for determining the presence or absence of the antibodies against

istle disease (ND), Mycoplasmosis (Mg) and Infectious Coryza (1C)

glutination antigens (ND virus. Mg. Hemophilus paragallinarum) can agglutinate

rythroeyles.

-> infection —> production of hemagglutination Inhibition antibody (HI antibody)

liilus paragallinarum in the serum of

infected chickens.

containing hemagglutination inhibition antibody erythrocytes + hemagglutination.......The hemagglutination was inhibited and blood cells were sedimented at

er of the bottom.

containing no hemagglutination inhibition, antibody erythrocytes

lutinat ion antigen the blood cells were agglutinated and spread over the

4S

i

\?

•rials.

iratuses.

lube 10 ml (inside diameter 10 mm)

agglutination plate with boles (SxlO boles).

s (0 5 ml. 1 ml, 5 ml. hole pipet)

ifugal separator.

lion syringe ( 10-20 ml).

ing solution

ological saline solution (0.S5% Nacl)

vsiological saline buffer solution

im Chloride (Nacl) 170 g

;sium Phosphate (K. HPOJ 13.6 g

im hydroxide (NaOH) 3.6 g

led water 1000 ml

;d the stock solution to 20-folds on using.

Erythrocyte suspension.

citrate solution 20 ml was put in a syringe of I/ 10 amount of the collected blood (for

nting blood coagulation).

cting the Blood.

eled a prescribed amount of blood from wing vein of healthy cockerels The blood

ollected from not one but two cockerels or more to be mixed.

ifijgation.

•d quietly the blood to the centrifuging lube from the syringe.

49

!•

m

:d physiological saline solution or physiological saline buffer solution of the 40 to 50

; the amount of the blood and blended well.

rifugated it with a centrifugal separator at 2000 rpm for 10 minutes

jved the supernatant with a sucker, added physiological saline solution of the 40-50

the amount of the blood and centrifugated similarly

ated the centrifugating procedure till the supernatant became transparent (at least .1

),

Red Cell suspension.

i the supernatant became transparent, sucked up the sedimented erythrocytes with a

e and 0.5 ml. of them was put on physiological saline solution in another vessel

was cleaned by passing it through physiological saline solution before using If

ocytes were not suspended uniformly but agglutinated or precipitated, the sample

ot used in the test .

rvation of Erythrocytes

emaining erythrocytes were preserved for several days by diluting with an equal

nt of physiological saline solution or ALsber Solution and keeping at 0-5 'C.

losition of ALsber Solution :

24.6 g

m citrate 9.6 g

m chloride 5.0 g

1200 ml.ed water

ilution was pasteurized at I 10’C for 15 minutes.

gglutinin (Antigen).

gglutinin (ND antigen) is commercially available. The commercial ND antigen was

ated with 0.1% formalin to prevent contamination by virus.

50

V

nail hole in an ampoule of the antigen was made

r opening the ampoule, poured I ml. of physiological saline solution to dissolve and

or the test after I hour.

m.

ecied the blood from the wing vein and centrifugated it and separated scrum

blood collected 1.0-2.0 ml

0.2 mlm

of Titer of Hemagglutination Antigen.

test was performed so as to measure the titer of antigen (hemagglutinin) lor

jgglutination inhibition (HI test) and to determine the dilution ratio of antigen

result showed that the dilution of antigen was judged light and the diluted antigen

used for HI test.

:Inrd Method :

Diluted the serum by two-fold dilution method.

Added antigen

Added 0.5% erythrocyte suspension.

Allowed to stand for 40-60 minutes and judged ( 1 7-25 C)

m dilution ratio at the final complete sedimentation wfas hemagglutination inhibition

•(HI value).

due was 20-folds in the above test

51

*

Inoculation Test.

2St was also performed in the laboratory for the confirmation and diagnosis of Foul

n pasteurellosis) in the laboratoiy and for this purpose pigeon was inoculated with

rial. Pigeon died within 4S hours in positive cases.

sis of Data.

s study fifteen years data starting from January' I97S to December 1092 was

ally the data was entered as it was in the Computer through QuatroPro program and

s placed in the Appendices 1-15 of the thesis.

Disease Outbreaks.

he raw data was coded into numerical form and then exported to Statgraphies an

alvsis Program, for further statistical analysis The data were grouped in frequency

and the yearly outbreaks of various diseases computed Data were /v+ 0.5

alues + 05 and then subjected to analysis of variance However, untransformed

recorded epidemics were tabulated and discriminated through DMRT (Duncan

:e Test).

nal Disease Outbreaks.

term, seasonal and secular changes are temporal trends that can occur

y, and may be mixed with random variation. In such circumstances, the various

be identified by statistical investigations. The most widely used method in

to detect temporal trends is time series analysis. A time series is a record of events

;r a period of time.

iques used to detect the temporal trends of disease epidemics were the calculation of

and regression analysis. Trend analysis provides simple methods to estimate the

he next period based upon recent performance in one or more preceding periods

this case was a month. The moving averages techniques were used in these simple

irrent-period performance based on the recent past.

52

*I

ng average, arithmetic procedure, was calculated. Moving average is based upon an

le value of a variable over the Iasi several variables Moving average was calculated

la :

V(i)

(I)

N

he number of preceding periods;

r the number of prior periods N included

iaverage;

or period forecast; and

ior period epidemic.

technique reduces random variation and mav therefore reveal underiving trends In

ige the first and the last elements of data set(s) could not be averaged In order to

s problem, the effect of seasonal variation was remov ed by calculating the Seasonal

h month The value of y for each month of a year was taken as a proportion of the

that year; these proportions were averaged for a particular month ox er the period of

a seasonal index for each month of the year. The results were "de-seasonalized" by

value ofy by the relevant monthly index multiplied bv 13

r Regression was applied to the analysis of time series The relation between the

; follows :

n r S F (2)

te number of outbreaks;

in months,

ept on Y, and

of line

er of observations used,

53

ition coefficient,

trd deviation from regression, and

:s.

Space Clustering.

space clustering is an interaction between the places of onset and the times of onset

'lie Poison distribution/ncgative binomial distributions may be applied in this type of

aylors1 power law technique was used for detecting time-space clustering Taylors'

scribes the sample variance as a function of the sample mean Mean and variance

id for each transact in each month and were used to estimate the parameters of

presenlative equation for the model is

ition purposes the above equations is derived to the following equation

B log m n _r s F (4)

S is the standard deviation and 113 is the mean based on log 10. a is the intercept on

; slope of line, n is the number of observations used, £ is the correlation coefficient.

ird deviation from regression and F is F-Statistics.

idity, Mortality, and Case Fatality Rates.

lorbidity. mortality and case fatality rates were calculated through QuatroPro

following formulae :

Number of sick birds

- ,\ 100e

Number of birds in flock

54

*

Number of dead birds

x 100ate

Number of birds in flock

Number of dead birds

v Rate \ 100

Number of birds manifesting

lhe disease.

55

CHAPTER - IV

RESULTS AND DISCUSSION

his study 15 years data from 1078 to 1002 was obtained from five districts of Sindh i e

yderabad, Nawabshah, Mirpurkhas and Sanghar which are rich in commercial broiler

joultry farms. The poultry disease diagnostic laboratories are also working in these

r last fifteen years and besides collection of the data on poultry diseases were also

n these diagnostic laboratories during this study

icational Level of ihe Poultry Farmers.

.as imperative to know the educational level of the poultry- farmers in order to assess

of commercial poultry farming in Sindh. The data on t he educational level of the

ners were collected on a survey questionnaire

,'se data are presented in Table I. These data showed that educational level of the

mers ranged from non-matriculate persons to graduate persons involved in the

Karachi out of 2300 poultry farmers. 50 were non-matriculate, 900 were matriculate.

intermediate. 700 were graduate and 550 were un-educated i e 2.2 percent people

n poultry' farming were non-matriculate, 39.1 percent matriculate. 4 3 percent

e. 30.4 percent graduate and 24.0 percent un-educated people were involved in poultry

Karachi.

Hyderabad district in 300 poultry farmers, 10 owners were non-matriculate. 100 were

•, 50 were intermediate, SO were graduate and 60 were un-educated i.e. 3 4 percent

olved in poultry farming were non-matriculate, 33.3 percent graduate and 20 1 percent

56

1

Total

Number of

Farmers

llii-educatedIntermediate GraduatePLACE Non-matriculate : Matriculate

Actual : AtActual •»/. AtActual : Actual • «»/At Actual . U/. Atit/At

2300550700 50 4 24 0Karachi 900 4 5i~> 59. 1 10050

30050 10 0 20.1Hyderabad 10 26.0 605.4 100 33 5 SO

i /

23525.5 45 19.2Nawabshah 15.5 609 3.9 85 36 1 36

17.4 202Mirpmkhas 50 27 27 57 I 14 S 5575 >>

167Sanghar 4565 21 o IS 05.0 58 0 50

Sindh 7 4 720 32041225 -i ow.'O 29 581 2.6 38.2 940

%

Nawabshah district 235 poultry farmers were involved in poultry business and out of

farmers were non-matriculate, 85 were matriculate. 36 were intermediate. 60 were

ind 45 were un-educated i.e. 3.9 percent non-matriculate. 36 I percent matriculate. 15 3

termediate, 25.5 percent graduate and 19 2 percent un-educated persons

Mirpurkhas 202 farmers were related to poultry farming business and out of these.

ere non-matriculate, 75 were matriculate. 30 were intermediate. 55 were graduate and

in-educated i e. 3 5 percent people involved in poultry farming were non-matriculate.

•nt matriculate, 14.8 percent intermediate, 27.2 percent graduate and 17 4 percent were

ed.

district Sanghar out of 167 total poultry farmers, the owners of 5 were non-matriculate.

matriculate, 22 were intermediate. 45 were graduate and 50 were un-educated i e in

0 percent non-matriculate. 58.9 percent matriculate. 13.1 percent intermediate. 27 0

iduateand 18 0 percent un-educated persons were involved in poultry farming

erall in Sindh province, 2.5 percent poultry farmers were non-matriculate. 38.2 percent

:. 7 4 percent intermediate. 29.3 percent graduate and 22.4 percent un-educated

ion the data were pooled on Sindh basis, it became clear from the fore described results

ijorily farmers were matriculate and graduates In-educated persons have also adopted

mint; business and low percentage of intermediate and non-matriculate people uere

i commercial poultry farming in the province. The reason of high percentage of

and graduate people involved in poultry farming was un-emplovment in Government

id lack of jobs in oilier agencies, people have therefore started poultry business

itli low-investment and gradually they have increased their business.

.* Structure of the Poultiy Farmers.

/as also imperative to know the age structure of the poultry farmers in Sindh so as to

merest of people of different age groups in poultry farming business The data on the

re of the poultry farmers surveyed in the present study are shown in Table 2. These

58

\PLACE : 18 to 20 yrs. 21 to 25 MS. 31 to 40 vrs. : 4 1 to 50 MS. : Total26 to 30 MS. :

: number: and above

: of: Actual : % Actual Actual Actual :. /II Actual : 11/ 4At . Fanners: % : % :

Karachi 250 350 15 2 450 10.510 9 500 21.7 750 52 7 2500

ui

HyderabadVO 40 13.4 50 60 20.016.6 70 23.3 300SO 26 7

Nawabshah 9.4T) 17.040 4S 20.4 25.5 27 7 23560 O.-'

Mirpurklias 9 519 i

16.5 19 840 50 24.7 20260 29 7ja

Sanghar 16 9.6 2S 16.7 5 5 20.9 40 24 U 1672S S4S

Siiulh 547 10 9 501 15 7 655 1 9.8 720 22 5-s • -i

J A 52041005

!*

ed tliat age-structure of the people involed in poultry farming in Sindh ranged between

•ears or above.

Karachi out of 2300 poultry farmers, 250 farmers were in between IS to 20 years of

rmers were in between 21 to 25 years. 450 farmers were in between 26 to 30 vears.

s were in between 31 to 40 years and 750 farmers were in between 41 to 50 years and

0 9 percent people were in between IS to 20 years. 15.2 percent were in between 21

1 9.5 percent were in between 26 to 30 years. 217 percent were in between 3 I to 40

2 7 percent people involved in poultry farming in Karachi were in between 41 to 50

_ÿ and above.

lyderabad 300 farmers were involved in poultry farming business and out of those

• were in between IS to 20 years. 50 were in between 21 to 25 years. 60 were in

to 30 years. 70 were in between 3 1 to 40 vears and SO farmers were in between 4 1 to

age and above i.e 13 4 percent persons involved in poultry farming were in between

ars, 16 6 percent were in between 21 to 25 years. 20 percent were in between 20 to 30

percent w'ere in between 31 to 40 years and 26 7 percent people involved in poultry

lyderabad were in between 41 to 50 years and above

lawabshah out of 235 poultry farmers. 22 were in between IS to 20 vears of age. 4S

ween 26 to 30 years. 60 were in between 31 to 40 years and 65 farmers were in

to 50 years and above i e 9.4 percent people involved in poultry farming were in

to 20 years. 17 percent were in between 21 to 25 years, 20.4 percent were in between

lrs, and 27.7 percent people were in between 41 to 50 years of age and above.

lirpurkhas out of 202 poultry farmers, 19 farmers were in between IS to 20 years. 33

veen 21 to 25 years, 40 were in between 26 to 30 years, 50 were in between 3 I to 40

0 farmers were in between 41 to 50 years and above i e 9 5 percent people were in

to 20 years, 16.3 percent were in between 21 to 25 years, I9.S percent were in

to 30 years, 24.7 percent were in between 31 to 40 years and 29.7 percent people

poultry farming were in between 40 years to 50 years of age and above.

60

u

strict Sanghar 167 persons were related to poultry farming and out of these farmers.

to 20 years, 28 had 21 to 25 years age. 35 ranged from 26 to 30 years. 40 were in

to 40 years and 48 farmers were 4! to 50 years of age and above i e 0.6 percent

in between IS to 20 years, 16.7 percent were 21 to 25 years. 20 0 percent were 26 to

0 percent were 3 I to 40 years and 2S.S percent people involved in poultry farming in

age 4 1 years to 50 years and above

he province basis, out of 3204 poultry farmers, 10.0 percent (IS to 20 vears). 15 7

to 25 years), 19 S percent (26 to 30 years). 22 3 percent (31 to 40 years) and 31 3

;o 50 years of age and above)

I Table 2 it appeared that the majority of the farmers invoked in poultry business

s to 50 years of aye and above followed by 3 I to 40 years age group

ibcr of the Ponlti'y Farms, Flocks and t tic Birds on Poultry Farms.

ev was conducted in order to record the number of poultry farms, number of docks

of the birds kept on these farms The data on the number of poultry farms, number of

d total number of poultry farms, is shown in Table 3

lata presented in Table 3 revealed that in Karachi, total poultry farms were 2300 with

; and total birds numbering to 28000000. In Hyderabad, total poultry farms were 300

locks and total birds numbering to ISOOOOO. In Nawabshah total number of the

is were 235 with 800 flocks and total birds numbering to 1400000. Similarly in

poultry farms were 202 with number of flocks and birds 600

Sanghar had 167 farms with 550 flocks and 800000 birds. Data included both the

Toilers. From the results it clear that Karachi had the highest number of farms and

:d by Hyderabad. Nawabshah, Mirpurkhas and Sanghar districts.

and 1000000

61

\Number of the BirdsNuinher of the FlocksPlace Numher of the Poultn farms

28000000Karachi 1 -10002300

IS00000Hyderabad 300 1000

M00000235Nawabshah soocr,PO

1000000Mirpurkluis 600202

Sanuliar sooooo167 550

Sinddh 3204 33000000|60>0

Disease : Number : Morbidity : Case•)//it : Mortality 41/

/II

: of Farms : per Farm : per Farm : Fatality

Coccidiosis 32 551216 27S 02 12S 030 22.0414. IS

Marek's Disease

Newcastle Disease

Chronic Respiratory' Disease

Fowl Pox

Infectious Coryza

Lymphoid Leukosis

Fowl Cholera

Gumboru Disease

300 25 30 12.25100 |S4 23 40S5 S6

24.75200 4X1087 24 75 34 0 1200 4S

630 702 23.005243 IOS.079 I I 181 18.804ov

55 213 T) yis21 00 03 803 10 07OJ

105 03 20 07 77 220403 10. 15 025

154 X2520 20.36 10 30 20.2375

81 548 08 20 i6 i 58 07 0 14 23 473

317 391 48 10 74 148 70 I 53O 44

Salmonellosis 1328 140.002 15 788 07 040 8 274 14 703

Colisepticaemia

Angara Disease

Fowl Typhoid

470 184 47 I I 85 80 700 S •'S 12 84

223 154 3 7 1 1 54 5 17 12 72108 0 1

4! 60 I 25 l» 70 40 25 7 4 25 08

95

fERIAL DISEASES.

inellosis.

us of Outbreaks.

of outbreaks of Salmonellosis in live districts of Sindh are depicted in

results for patterns of Salmonellosis presented in Table 4. showed that during 15

arms out of 3204 farms under surveillance were affected with Salmonellosis and

this disease per farm was 207.94S (75 654 %). From the data it appeared that the

er of outbreaks were reported from Karachi 3920 (261 333 average pei year)

(yderabad 1328 (88.533 average per year), Nawabshah I32S (SS 533 average per

khas 1 1S2 (75.2 average per year) and Sanghar 902 (60 133 average per year). The

r of outbreaks were however recorded in Sanghar The overall average number of

year in all the districts were 577.333. Outbreaks of Salmonellosis were reported

e year and the disease occurred in the birds of all ages Apparently observed number

Joes not seem to be high yet the problem existed in the province. In many cases the

>t report the disease outbreaks to the laboratories that is why the cases on province

;em to be so high.

ortem Lesions.

ises brought to various laboratories were subjected to postmortem, the typical and

es showed the lesions like: arthritis (Figure 2), morbidity of ovary in adult chicken

id liver with pin-point necrotic foci (Figure 4), the lesions are reported by other

ie Salmonellosis.

idity Rate.

rsults for morbidity rate of Salmonellosis presented in Table 4 showed that the

per farm was 140.002 (I5.7S8 %).

lity Rate.

rsults for mortality rate of Salmonellosis is also presented in Table 4 and the

of Salmonellosis per farm was 67.946 (8.274 %) recorded from 132S commercial

of different districts of Sindh during 15 years.

64

igure : 1

hunker of outbreaks of .Salmonellosisin Sindh

lu'Oiiks

\yt\ 1

Districts

Hyderabad

li:;:::! Sangliar

L

___i MaunliShahi Karachi

i Mii'i'iuKIIAS

m)

65

!,

*

;• "Vÿgps4p f:/'

:-V

i*30P M/ÿÿ

.

‘ v -T -»*•*.-/•-.

mwm.....mmmM v?

|

SrljS

: <v•i__

:

litet-Tri

— &5S

}iÿy

Tvoicnl lesions of Arthritis in S-imorp[ Losu-

LTjJJ- V “_r.r * j

mwmiJvA

,.,w_-

££*1

'•: -.

V! Pr* ;

Ptÿllfete'

wc•X*

RSr-srj

Ly"

Morbidity of ovnry in Salmonellosis

6 G

»

c

S

ftS

i%&

ST

iver with pin-point necrotic foci in So1mono1 iosis

4«*CSSS

Sr»S

fiL:>:ÿÿB!9

*5

S3ilias #3

tena

3BiS3G£ K-5 395

bi3

- : '

JHMmMr-sac inflammation in Chronic Respiratory Disease.

67

T!

;it results showed that Salmonellosis is a high morbidity with low mortality rate.

i

ility Rate.

case fatality rate are summarized in Table 4 The results revealed that the

wed 14.763 percent case fatality rate per farm in 15 years of data recorded from

poultry farms of Sindh.

' Outbreaks.

trends of occurrences of Salmonellosis from 1*378 to 1992 in poultry farms of

ented in Figure 5. The regression line showed a rising trend of the disease

)f occurrences of Salmonellosis in poultry farms of Flyderabad. Nawabshah.

are summarized in Figures 6, 7. S and 9, respectively The regression

rising trend in those districts.

rasing (rends of outbreaks reveals unsatisfactory management and disease

ires and the situation calls for more drastic disease control measures on

rv farms of Sindh.

view of literature suggested that Salmonellosis (Paratyphoid) was widely

lisease of economic importance, in miscellaneous birds, in the second and third

entury. Not until the middle of the century, however did it begin to come under

This came about largely through increased awareness that disease in man had a

tion in poult rv. Contributing also was extensive work on Salmonella typing

early |930's at the university of Kentucky under the leadership of Dr Philip R

h, 1977).

i major food source, has long been recognized as one of the principal source of

tions in man. A recent survey in Canada (Duitschaever. 1977) found a

e of about 34.8% of retail chicken products.

te of Salmonella contamination of carcasses is said to be due to contamination at

>cessing plants (Timoney et a|., 1970, Simmons and Byrnes. 1972; Me Garr.

onella serotypes found in processed carcasses and processing plant environments.!

r!

68

III!!

r

ire : 5

Trends of Salmonellosison poultry farms of Karachi.

T

7A :

79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Smooth RegrData

ill

69

r

:e : 6

Trends of Salmonellosison poultry farms of Hyderabad.

X

V w

79 80 81 82 83 84 85 86 87 88 89 SO 91 92

Years

Data — Smooth Regr

70 V ;:

F::

re : 7

Trends of Salmonellosison poultry farms of Nawabshah.

79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data “ Regr— Smooth

I

71

I

ire : 8

Trends of Salmonellosison poultry farms of Mirpurkhas.

Jr

-V

79 80 81 82 83 84 85. 86 87 88 89 90 91 92

Years

Smooth —:*— RegrData

72

T-

II

:e . : 9

Trends of Salmonellosison poultry farms of Sanghar.

JgL

t

APc

79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Smooth —»*— Regr.Data

i

73

r-

19

)nes found on broiler rearing farms (Woodburn and Sladelman. 1968, Simmons

72; Bains and Mackenzie, 1974). Timoney et a!., (1970) showed that serotypes

carcasses changed with the Hocks being processed, and concluded that the

'ith Salmonella in processing plants was introduced on birds from infected Hocks

.ÿnee of Salmonella infection in poultry was difficult to ascertain, since birds might

hout showing clinical disease. Surveys in various countries have shown an

g from 0 1% to 5% (Gordon. 1971).

of lloor litter has been shown to be a reasonably accurate and practical method

fected tlocks (Olesiuk el a], 1969; Snoeyenbos gt a] , 1969; Snoeyenbos, l(>7l).

to Olesink et a], (1969). lloor litter is more dependable than serological tests.

nd nest litter.

e et a],, ( 1990) reported over the past 5 years the number of Salmonella enteritidis

mans have increased on both sides of the Atlantic ocean 7'he WHO salmonella

ta for I979-S7 were reviewed and show that S enteritidis appeared to be

t least the continents of North America, South America, and Europe, and mas

S enteritidis isolates increased in 24 (69%) of .15 countries between 1979 and

. only 2 (10%) of 2 1 countries with data reported S enteritidis as their most

nella serotype; in I9S7. 9 (4.1%) of 21 countries reported S enteritidis as their

serotype. S (89%) percent of 9 were European countries Although the reason tor

rase in not yet clear, investigations in individual countries suggested it was related

i of eggs and poultry which harbor the organism.

s, in the study under discussion, outbreaks of Salmonellosis were reported from

nmercia! poultry farms in five districts of Sindh and the disease was well diagnosed

disease diagnostic laboratories. The morbidity rate per farm of this disease was

l, the mortality per farm was 8.274 percent. The disease showed comparatively

ty rates than the mortality rates. These results suggested that the disease manifest

with low mortality and the patterns and trends of Salmonellosis on commercial

of Sindh from 1978 to 1992 was analyzed in this study and according to the

vsis, data occurrences of Salmonellosis showed a rising trend all over in Sindh

reasons of widespread occurrences of this disease at the farm level could be same

y the various foregoing authors. The rising trend of this disease obtained in the

warrants more drastic disease control measures at hatchery as well as at poultry

74:

'I

Tic Respiratory Disease (CRD).

ns of Outbreaks.

items of outbreaks of Chronic respiratory disease in Sindh are depicted in Figure

from these data that the highest number of outbreaks of this disease were reported

8 (127.266 average per year) followed bv Hyderabad 46.7 (42.4 average per year).

1(42 4 average per year). Mirpurkhas 499 (3.1 266 average per year) and Sanghar

ge per year). Outbreaks of CRD were generally reported in winter season and the

ltlv occurred after the middle chick period and was mainly diagnosed from pullets

that highest number of outbreaks were reported in Karachi, and the lowest in

n average 272.266 outbreaks per year on province basis

>rtem lesions.

osl conspicuous lesions observed on postmortem examination were air-sac

Figure 1 1), joint-membrane inflammation (Figure 12). congested lungs with vellow

ilarged liver having thick-white covering.

lily Rate.

itv rate of Chronic respiratory disease (Table 4) showed that 616 farms were

he disease during 15 years. The results showed prevalence of this disease per farm

>9 261 °o) and the morbidity per farm was 241 702 (21.995 %)

ity Rate.

lilts for mortality rate of Chronic respiratory disease are presented in Table 4 The

)f CRD per farm was 11.181 percent recorded from 616 commercial poultry farms

tricts of Sindh during the period of study. The disease showed high morbidity with

ate.

atality Rate.

i case fatality rate are summarized in Table 4. The results revealed that the Chronic

ease showed 18 894 percent case fatality rale on the pooled data from 616

iltry farms of the province.

75 >iv

: 10Lgure

' Number of outbreaks ofClironic Respiratory Disease in Sindh

oul.brenUs

ij

mm

DIKIIIHS

lljriernbnd

S’nngliar

RH KnrnHii

MirpiirKlirtB

(CJ NnnnbShnh

ID2)

76

*.

i

r}

LL

mHs'H

:

\

»rk w •

Ik»

r4'

Joint-membrane inflammation in

Chronic Resoiratory Disease.

V» '*.ÿ4

:r

i!

. *•

in •A.r*

** i

£

% A £

f#r' &J > ,*

i.r-; ...

;/ÿ* r ! !.

V sii?2fr-'JirlS

1

L?V.4

pi'

'Lx?.fr

* ‘f®;

l-

}evere pericarditis , perihepatitis and airsacculi tis

itin Colisepticaemia. H!u!

ill-7 *7

;

Is of Outbreaks.

lines drawn on the data of CRD on commercial poultry farms of Karachi.

slawabshah, Mirpurkhas and Snnghar are shown in Figures l.\ 14, 15, 16 and 17

The regression lines showed rising trend of occurrences of the disease in all the

Jisease is caused by Mycoplasma gallisepticum (MG) which is considered as a

thogen of chickens and turkeys. Mycoplasma gallisepticum (MG) is one of the

ise agents in the commercial layer industry. It has been estimated that MG-infected

nearly 16 fewer eggs per bird than uninfected hens, resulting in a potential annual

to the V.S. layer industry of $I IS million (Carpenter et. fl].. 1979; Carpenter et a] .

*mic losses from MG infections results due to mortality, reduced weight gain and

y. decreased egg production, and increased condemnations. Various antibiotic such

e tetracyclines, spectinomycin and lincomycin have been used to minimize losses

J (Olson et a]., I960; Olesuik et ah, 1964; Hamdy and Blanchard. 1969, Ose et a!

in. I9SI)

dh province, on the basis of present study it could be said that the disease is of

economic importance. The reports from other parts of the world also support the

e present study. The disease is reported to be of continuing economic concern in all

Jnited States (Yoder, 1984). Vaccination of replacement commercial layer pullets

product or live culture of MG has been used to reduce egg production losses.

>sts, and mortality associated with exposure to field strains of MG (Carpenter et ai

)n and Kleven. 1984; Kleven e( a! . 1984; Yoder ct. ah. 1984). It has been

that vaccination with an oil emulsion bacterin does not adequately protect against

tization by MG (Yoder et a! , 1984; Talkington and Kleven, I9S5). nor does it

educe the numbers of organisms in the tracheas of infected chickens (Kleven. 19S5)

with the live vaccine have demonstrated that vaccination with F Strain significantly

;olation rate of pathogenic MG strains from the tracheas of heavily challenged birds

I Kleven, 1981)

78

*.

<j

Figure : 13

Trends of Chronic Respiratory Diseaseon poultry farms of Karachi.

w

t7

M

78 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Smooth Regr— Data

79 i-!

it

I

H

'igure : 14

Trends of Chronic Respiratory Diseaseon poultry farms of Hyderabad.

77

Vt

-fI

T T T T T T T TT T T T T

78 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data Smooth - *- Regr+

80 !i

\

t

Figure : 15

Trends of Chronic Respiratory Diseaseon poultry farms of Nawabshah.

7/ \

0

0\s

0

078 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data Smooth * Regr+

\

81'}

li. >

¥

Figure : 16

Trends of Chronic Respiratory Diseaseon poultry farms of Mirpurkhas.

•f

*•

/

+

r T T T T 7

78 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data Smooth * Regr+

82 i

f

;

*

gure : 17

Trends of Chronic Respiratory Diseaseon poultry farms of Sanghar

'4- -4-

7

L

z.v+r

+

78 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

7T

Data Smooth *-•- Regr.

r83

•I

I

('oliscplieaomin.

Patterns of Outbreaks.

flie Figure 18, depicts the pattern of outbreaks of Colisepticaemia in live districts of

i appears from these data that the highest number of outbreaks had occurred in Karachi

)4.0 average per year) followed by Hyderabad 470 (31.3.1.1 average per year) and

;hah 470 (31.33.1 average per year) In Mirpurkhas averages cases per year were 20.67

otal of 400, similarly, in Sanghar district mean yearly cases were 22.67 with a total of 340

)utbreaks of Colisepticaemia were reported throughout the year and the disease occurred

g and mature birds. The overall average per year in all the districts figured 206. In district

r the number of outbreaks was the lowest probably due to small number of farms. Thus

of disease occurrence goes with the number of poultry farms which were at tbe lowest end

bar in comparison to the other districts.

Postmortem Lesions.

Severe pericarditis, perihepatitis and airsacculitis (Figure 19) were the common findings

‘d on postmortem examination of Colisepticaemia affected birds. In most cases pericarditis

ihepatitis with white deposits on the heart and on the liver (Figure 20) were also observed.

fected birds showed liver with (Figure 21) severe hepatitis and urate deposits and white

ion on the heart as well as on the liver (Figure 22) Swollen and congested liver affected by-

showed severe hemorrhagic spots on it's surface (Figure 23).

Morbidity Rate.

The results for morbidity rate of Colisepticaemia are presented in Table 4. 470 farms were

affected with the disease and the prevalence rate of the disease per farm was 264.86 (68.72

1 the morbidity per farm was 1 84.47 ( 1 1 .85 %).

Mortality Rate.

The results for mortality rate of Colisepticaemia are presented in Table 4. The mortality

:r farm was SO.709 (5.25 %) recorded from 470 commercial poultry farms of the province.

84

h

Figure : 18

Number of outbreaks of Coliscpticacmiain Sindh

onihn'nhs

0.

i

III ..mm m

m.-ti i.-i «

M Hyrlprnbnil

Snuglinr

?? 1 I\’ilMrlii

VMM Milj'KiKli.lK

tUl Nnifnl'Sli'ili

2)

85

mtImmlllSS

5»5

MBS IS

issiWWtXIfllJSilljiP «8

USivs

IIw3fcc

VBI»

&&0

MSHIIIIE

*:? as£3

m mmm mm

PI>ÿ*•;- -JJ*I ews S.3S33

and perihepatitis with white deposits onionrd111s

the heart and on the liter in CoIiseo11caornIa.

4ÿta*»'.ÿ•.%-'-v*r.

m

2

mmhirf-'/

\-

mmm

m

Liver showing severe hepatitis with urate

deposits in Colisept icaemla.

80

‘i

>

"if'll

£•/&ti g;1

14* j®;m

' . : i

>i . p.

•y-v•-ft,,

.fif,V *'ÿ

ii V?1'!1- l%'*« .: >

iSMl•i - T

iHU

m.mmim!wmmmW1

S3

f.

*v;

jjT.-,! ‘

ite deposition on the heart and on the liver inColisppt icaemin affected chicken.

r l;A - t*

/-

7t‘

jfljfpWis#f*V

r,V_".

pIII;« .'$m

siipÿ'

feSSl

lien and congested liver with severe hemorrhagicspots due to C.coli.

«.87

B

Case fatality Kale.

Data on case fatality rate are summarized in Table 4 These results revealed 12 84 "o case

rate from the above reported commercial poultry farms.

Trends of Outbreaks.

Trends of occurrences ol" C’olisepticaemia in commercial poultry farms are presented in

s 24. 25. 2b. 27 and 2S The regression lines showed a rising trend in all the districts

mg that this affection is on a continuous rise and warrants strict preventive measures

Escherichia coli is regarded as member of the normal bowel llora of mammals and birds.

strains are pathogenic due to (lie acquisition of virulent factors (Elvvell and Shipley,

In birds. E. coli infections cause many clinical manifestations (Gross, 1984). the most

on being airsacculitis, pericarditis, septicaemia, and death (Sojka, 1965) Similar

.'stations were recorded during the postmortem examination in the present study

According to Gross (1984) and Sojka (1965), E. coli infections caused many clinical

.'stations, the most common being airsacculitis. pericarditis, septicaemia, and death. These

-is tally with those of the present study as perihepatitis and airsacculitis were the common

rs observed in postmortem examination of Colisepticaemia affected broilers. In the present

outbreaks of Colisepticaemia were reported in all the districts of Sindh under study in

g degrees and it was observed that Colisepticaemia was of great economic significance on

immercial poultry farms of the province. The results fall in agreement with those reports

( I97S), who observed that Colisepticaemia was responsible for significant economic losses

;ulture in many parts of the world. Many other workers have reported that Colisepticaemia

esponsible lor significant economic losses, although the mechanism of pathogenicitv of

; of E. coli that were potentially pathogenic to birds was not fully understood (Elvvell and

v, 1980)

88

gure : 24

Trends of Colisepticaemiaon poultry farms of Karachi.

r

7

Tr T T TT T T

78 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

* Data Smooth * •• Regr+

;

89

w

jre : 25

Trends of Colisepticaemiaon poultry farms of Hyderabad.

>r

/

m-

TT T T T T T T TT T T T

5 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Smooth — Regr— Data

90

i:

f!

gure : 26

Trends of Colisepticaemiaon poultry farms of Nawabshah.

v

•-jj.7

i T T T T T TT I T TT

'8 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Smooth Regrf— Data +

:

91:

juÿre : 2 7

Trends of Colisepticaemiaon poultry farms of Mirpurkhas.

P..../

—ifk

TT Tr T T T T T T T T T T T

8 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

— Data Smooth —: Regr+

92

1

jure : 20

Trends of Colisepticaemiaon poultry farms of Sanghar.

"-4NrS/

r /

T T T TT T T T T TT T T

r8 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Smooth Regr.Data +

93

i

*

ml Cholera (Avian Pasleurcllosis).

Kerns of Outbreaks.

ie patterns of outbreaks of Fowl cholera in live districts of Sindh are depicted in Figure

data showed that the highest outbreaks per year in Karachi was 245 (lb 2 average)

by Hyderabad SI (5.4 average). Nawabshah SI (5 4 average). Mirpurkhas 55 (5 555

nul Sanghar 5b (2.4 average) Outbreaks of Fowl cholera were reported throughout the

he disease was mainly diagnosed in mature birds. The lowest edge of outbreaks were

n Sanghttr (52.955).

Lesions.

•How nodules, white necrotic lesions and hemorrhages on the liver and pin-point

ics on tire heart were recorded during postmortem examination (Figure 50) and

lilt with hemorrhagic lesions (Figure 51) were also commonlv occurring lesions

n most cases in the present study

orbidity Rate.

ita summarized in Table 4 revealed that SI farms were affected with the disease

illy prevalence rate of this disease war. 507.55 (49 05 %) and the morbiditv rate \va>

) lb To)

ortality Rate.

ie data in Table 4, sliowed that the mortality rale of Fowl cholera per farms was 15S.b~

This disease behaved tobe a disease with high morbidity with low mortality

ise Fatality Rate.

ita summarized in Table 4 revealed that the disease showed 25 475 percent case latalilv

data recorded from 81 affected commercial poultry farms in the five districts under

ends of Outbreaks.

end lines drawn on the data of Fowl cholera on commercial poultrv farms of Karachi.

.1, Nawabshah, Mirpurkhas and Sanghar are shown in figures 32, 35, 34, 35 and 56.

Iv. The regression lines showed rising trend of occurrences of the disease in all the

94

i.

8

Figure : 29

NIIISIIMT of oul luoaks of Fowl hhoiora

in Sindh

OulIn ('jil.s

m1SII1! WMmM'-:. . \ .

Disl rids:

Ed M-:.vr:,I.Sh->liI.sirai 11i

Mii| MI Mm';

19!):F)

95

? •

t .1- •• •.

/':-a

’ /jS&fig% ;

V

vM .

c,:|5 A . * t :

snia

-A - •iv1£'ÿ

-1 4.v:•* m,m

1 \\v .

fliM 9' .P Mx& '<

I-’-: 1m?fci v:«ÿje

immitii:+

i Mi'

m %

PfPPSiEt-SP6: r •H

i

OK nodul PS , white necrotie lesion end homorrhaoeo the liver (A1 and pin-point hemorrhages on the

heart l C an Fowl Cholera.

/> +ÿ>AÿjyrJÿri fc'.Vilvÿr.ÿKÿ i

t

ii;y.i C1

- tfs- •-ÿ .;$ 4$'

flaaU £ m

m m% -iJ:i

* mim-

hr

mj.nal fat with hemorrherjic lesions in Fowl Cholern.

96

•’igure : 32

Trends of Fowl Choleraon poultry farms of Karachi.

78 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data Smooth —*— Regr

97

jure : 33

Trends of Fowl Choleraon poultry farms of Hyderabad.

z

3 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data Smooth Regr

98

>

Figure : 34

Trends of Fowl Choleraon poultry farms of Nawabshah.

3m

3

3

3 -W

s I/5 /ÿ--

3

3“Br-

78 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Smooth Regr>— Data

99 V

f

iguf-e : 35

Trends of Fowl Choleraon poultry farms of Mirpurkhas.

,.*r'*r"

78 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

- Smooth Regr— Data

100

•h

igure : 36

Trends of Fowl Choleraon poultry farms of Sanghar.

/

78 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data - Smooth Regr.

101

%

in Sindh according to the statistical analysis, data on occurrences of Foul cholera

sing trend during the period of study

ai ding to reports of many workers Fowl cholera, caused hv Pasteurella muhocida .still

isease of major economic importance despite more than 100 years of research have

>ades and Rimler. 1085) Before the avirulent C’lemson ldiversity { C'l') strain of

miltocida was discovered.

icute outbreak of Fowl cholera in one-month old chickens was investigated by Yadav

) Pasteurella gallmarum was isolated in pure culture from the heart blood of two

of the isolants on experimental inoculation was found to be non-pathogenic for

j and chickens. It did not provide protection in rabbits against a virulent strain of P

‘his was reported to be the first record of the isolation of P gallinarum in India

terature reviewed it is reported that mortality in turkeys due to Fowl cholera could

In the present study the disease was reported from all t lie districts under study where

lily rate per farm was 20.16 percent, and the mortality per farm was 0 14 percent

mortality rates are lesser than those reported hv Rhoades and Rimler ( 1985) in turkey.

y of the trends showed a rising trend of this disease on the poultry farms of the

102

¥

tions Coryza.

ns of Outbreaks.

37 shows disirictwise data on patterns of outbreaks of Infections coryza from 5

of Sindh. From these data it appeared that the different districts under study showed

ns of the disease Outbreaks of Infectious coryza were reported throughout the year

;e was diagnosed in the chicks as well as in the older birds. The highest number of

e reported from Karachi 139S (93.2 average) followed by Hyderabad 463 (30.866

cabshah 463 (30.866 average). Mirpurkhas 365 (23 733 average) and Sanghar 2~3

•) The lowest number of outbreaks were recorded in Sanghar and the overall

[breaks per year on pooled data for all the districts was 196 866

ortem Lesions.

ng was the first sign of Infectious coryza reported by the farmers On laboratory

he swelling of the face and wattles (Figure 38), soft swelling of the eyes, face and

re 39) were commonly seen with the atrophy of the ovarian follicle during

xamination

idity Rate.

jsults for morbidity rates of Infectious coryza are presented in Table 4. These

ed that in all 463 farms were affected with the disease. The prevalence rate per farm

' I 74 %) and the morbidity rate per farm was 165.03 (20.67 %),

ility Rate.

depicted in Table 4, showed that the mortality rate per farm was 77.22 (10 %)

i the data obtained from 463 commercial poultry farms These results suggested that

d high morbidity with lesser mortality rates

Fntalitv Rate.

.•suits showed 15 625 percent case fatality rate when the data were pooled for 461

jultry farms of Sindh (Table 4)

103

m

37cj ur e :

Number of outbreaksot Ini'eetiuus Coryza in Sindh

i ( breaks

•- Ii

-T

:4fTv; r>L ’t"T A —\ ~

:

Districts

Ficurc

IA'AVV.1 Hjilcrabad

Snngliar

EZ] N.'uv;il) SliahKru'u’lii

Mii'l'iir Ktuis

19U2)

104

‘1

m

w-m&

mm mmm m

s H

*:»

WBOT

Swell inn of the face and wattles inInfectious Coryza.

mmm mm mm•••;•

S.

m mmme?g

ii

•v

Soft swelling of the eyes, face and sinuses inInfectious Coryza:

105

r

Js of Outbreaks.

egression lines shown in Figures 40, 4i, 42, 43 and 44 for Karachi. Hyderabad.

Mirpurkhas and Sanghar respectively, showed rising trend of the occurrences of the

eview of the scientific literature further showed that the initial reports of (Nelson.

n. 1938) on the etiologic agents of Infectious coryza led io recognition of the

»f mycoplasma in respiratory disease in chickens.Hemophilus gallinarum (HGt was

a complicating agent in the type III, or complicated, coryza. According to latter

jlicatcd coryza has been reproduced experimentally with Mycoplasma gallisepticum

IG) in combination (Adler and Yamamoto, 1956. Kato. I%5). However, there had

slished reports on this complex disease. The absence of case reports suggested that

coryza was either relatively rare or that might be unrecognized due to the nature of

try management. In many other countries, however, there are indications that the

»e the case.

at trends have been toward returning to multiple-age- poultry operations under these

:h uncomplicated and complicated coryza are a potential hazard. According to Adler

>to ( 1956) and Knto ( 1965), complicated coryza has been reproduced experimentally

asma gallinarum (MG) and Haemophilus gallinarum (FIG) in combination but in the

y. Infectious coryza cases reported from all the districts of Sindh under study

the laboratory' by isolation and identification that Haemophilus gallinarum was the

concern. Patterns and trends of this disease on commercial poultry farms of Sindh

/ed a rising trend which necessitates more research to be conducted on this disease

106

*.

: 4 0ure

Trends of Infectious Coryzaon poultry farms of Karachi.

JK

r z

z"K

T T TT X T T r T T TT T T T

79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Smooth — Regr~ Data +

*107

re : 41

Trends of Infectious Coryzaon poultry farms of Hyderabad.

X

pV

*-

IXTT T T T T T T T T T T 7 T

79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

— Data Smooth —:*— Regr

I

J

i108

I

»«

gure : 42

Trends of Infectious Coryzaon poultry farms of Nawabshah.

i

£ \

51

/

'

//

!/

rz

Tr T T T T T T T T T T T TT

8 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data Smooth Regr+

*.109

r

re : 4 3

Trends of Infectious Coryzaon poultry farms of Mirpurkhas.

I-j

X

79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

m

Smooth * - RegrData

no

p

l'e : 4 4

Trends of Infectious Coryzaon poultry farms of Sanghar.

*\i

\1

\ i

.l

fN

___.ÿr +

-*+ÿ

O,r+T1

w \ - :; !+ÿ

.*T' :,-K'

\.>r '

*- *\

r T TT

79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Smooth Regr.Dataj

i

i

111

vl Typhoid.

Icrns of Outbreaks.

m Figure 45. it could be seen that the highest number of outbreaks were reported from

:.i (8.2 average per year) followed by Hyderabad 41 (2.755 average per year).

41 (2.755 average per year). Mirpurkhas 16 (1.066 average per year) and Sanghar 6

e per year). Fowl typhoid was reported throughout the year most outbreaks occurred

batched young birds.

tmorlcni Lesions.

lrged liver with small necrotic foci, enlargement of the spleen and kidneys and enteritis

rior small intestine with ulceration were the characteristic lesions of Fowl typhoid

this study during postmortem examinations

rbidity Rate.

le 4 showed that, in Sindh, 41 farms were affected with Fowl typhoid and prevalence

disease per farm was 106 575 (45.50 %) and the morbidity rate per farm was 66 125

vi tality Rale.

mortality rate per farm was calculated to be 40 25 (7 40 a/o). These results showed

yphoid had higher morbidity with lesser mortality.

re Fatality Rate.

: results revealed that 25.08 % was ease fatality rate computed on 15 years of data

om 4 1 commercial poultry farms of Sindh (Table 4).

of Outbreaks.

nds of occurrences of Fowl typhoid for a period of 15 years (1978-1992) for Karachi.

. Nawabshah, Mirpurkhas and Sanghar are shown in Figures 46. 47, 48. 49 and 50.

v. The trend of regression line was parallel in all these figures indicating a secular trend

ice of this disease upto 1992, and thereafter it has shown a declining trend in Karachi

1 12

H

gure : 4 5

Number of outbreaks of Fowl Typhoidin Sindh

Ibreaks

Distrids

LJD NawahShahkWWM Hyderabad

llii::] .Saiigliur

9 Karachi

% Mirpiij'Kiiiib

1992)

113

»,

ri

• : 46

Trends of Fowl Typhoidon poultry farms of Karachi.

Ii

\i

*+N

X

I -K

£r—X ---x--x-xx--x-

\»------*'9 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

T TT T T

!

— Smooth RegrData

114

re. : 4 7

Trends of Fowl Typhoidon poultry farms of Hyderabad.

*

;

I

-x-x— Jk-xX-X- X -X

+

-i-m-—m—»79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

-m m W

m~ Data Smooth — Regr

115

: 48

Trends of Fowl Typhoidon poultry farms of Nawabshah.

I//

/

'/-K/ k*1

/ N-e->•- 4k 4k 4k 4k 4k

-k

1-i »--*» *----»9 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

— Data Smooth — Regr

;

: J

i

v'

116

r

: 4 9

Trends of Fowl Typhoidon poultry farms of Mirpurkhas.

i

-k

\—5K- -X- xc-Xr X-tf X;

1

\\.....-K •

1 /m-m w— —m—m— — --1--r'9 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

*— Data - Smooth —*— Regr

117

1>

c e : 50

Trends of Fowl Typhoidon poultry farms of Sanghar.

\t

+.\

-*ÿ

l \

\/ +'K- ~*ir -*r -*r -*ÿ-5rr

\/

+ r

1

/\m-i-P-P-—m-*-----m-p-P

79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data Smooth ~ * - Regr.+

;

118

r

typhoid is a septicaemic disease of domesticated birds The course may be acute 01

he mortality moderate or very high, depending largely on the virulence of the inciting

Imonella gallinarum (Hall £t af. 1949; Pomeroy, 1972)

review of literature further revealed that the Fowl typhoid is worldwide in

The disease has been of considerable economic importance in United States (Hall and

SI; Pomeroy. 1972) especially during 19.19-46. when outbreaks in chickens and

ased dramatically in number. It was considered one of the greatest disease hazards to

iduslry along the eastern seaboard (Pomeroy, 1972) In 1975. 16 cases were reported

Stated (AAAP disease report summary. 1975) The dramatic drop in fowl typhoid

is related to the Pullomm-lyphoid control program (Pomorov. 1972) of the National

ovement Plan in that country. The similar type of programme may prove to be

control of this disease in this country' too.

;

r, this study is concerned. Fowl typhoid was reported in all the commeicial poultry

hout Sindh province with moibidily and the mortality per farm was 9.70 and 7 40

ectively The results of the present study showed low to moderate mortality and

es. these findings are in line with those reported by Flail el. al . ( 1949) and Pomeroy.

i

I 19

m

AL DISEASES.

1 Po.v.

crus of Outbreaks.

data depicted in Figure 5 1 showed (hat (tie highest number of outbreaks uere

Snnghai 175 (I 1 600 average per year) followed by Karachi 159 (10.0 average per

jabad 55 (1666 average per vear). Nawabshah 55 ( 5 666 average per year) and

were I 1 (0 7.15 average per vear) Fowl pox was reported throughout the vear and

ccurred in chicks and also in adult birds. The lowest number of outbreaks were

in Mirpurkhas and the average number of outbreaks of Fowl pox per year in all the

10 111

mortem Lesions.

various forms of Fowl pox were encountered in the present study The postmortem

ineous form (Figure 52). gasping in membranous form (Figure 51) and combination

; form (Figure 54) which was the most common lesion and caseation in larynx were

-d in some eases (Figure 55) It was observed that in "wet pox" cankers were

the membranes of mouth, throat and windpipe (figure 56) and in "dry pox" brown

I as small, rapidly growing white bumps, appeared on bird's comb, face and wattles

oidily Rate.

'esults regarding morbidity rate of Fowl pox are presented in Table 4. 55 farms were

i Fow4 pox and prevalence rate per farm was 107.74 (54 85 %). The morbidity per

> 85 (21,06%).

aJity Rate.

esults on mortality rate presented in Table 4 showed 91 891 cases per farm ( 10 97

from 55 commercial poultry farms of Sindh. The results suggested that this disease

lorbidity rate than mortality rate. It could be concluded that being a viral disease it

morbidity and mortality rate.

120

e : 51

Number of outbreaks of Fowl Pox

in Sindh

.V - — I'll?r..V "r.’27 j

pil/fey -w

\iVv.Y,\\rtiV.Vil\i!?

hiylrit.’lH

E

_____U N:k v. :i|.Sli:tli[ÿ•:ÿ,. -.1 111.lrr:il>:i<l

Snin;li;ir

!.:<r:n hi

Mitpfit Kh-v

92)

121

>•

* v*L >;

(ÿ) r

A #)

> I;.M

ss

• :

i.V'.rIt

r-':

LP .5lajns of cutaneous form of Fowl Pox.

V.

i

\ Tj

\ L?)*» .»

>

Gasping svmtom in membranous form of Fowl Pox.

122

» . ; :•

v yST&-.-.'V fs:" ; '.1

# erf. V “ÿ '-0 *

!

Silicas--'

L-

,

O'" -

'Us;>wi

r.‘

--ÿÿÿ

L r .•

ill.1

3tm'-z mw ‘v

3 »iV

R& V'ÿvji -m 13?

5L-VSy,rSft 1’ÿ• J”:H

--J- A:'"m*Mv-;4

,ÿm

.os «?-"'-ftiV.

K":•y

V' • . V- *

'omb L n a tlon of cutaneous form and membranous form

in Fowl Pox.

&tS-

*1

•'*

-t

-Vr •

.ÿÿ.

m •-«» -

, « J w

• ;Hr

/ V-&

Lit-- £<% r>.-7

~.ir'

m*Jt&UA

L, 1

I

t* i.

• 1 M*

-Cirij

-ÿ - ' .>-J

Caseation in larynx in Fowl Pox.

123

ft

w,itf*'r «

j

1 / i‘--v

-f' ,i. Y .

/

1% ..-•%. t,t(

*

V * -»SJ-ta

Cankers lmfoeded in ths membranes of mouth,throat and windpipe? in we t form of Pox.

phifpIMiaiaS

-••M-lf!ste

pi. -•

*M

0t 'ir

ivj•.TV

sifig:

h/V { *'ÿ«_:

S.

#-j

Brown scabs st<3rt as small, rapidlygrowing whits bumps i" ,!dry Pox".

124

ntality Rate.

suits summarized in Table 4, revealed that the Fowl pox showed 22.225 percent

te

s of Outbreaks.

. of occurrences of Fowl pox in Karachi. Hyderabad. X'nwabshah, Mirpurkhas and

how n in Figures 5S. 50. 60. 61 and 62 respectively The regression line showed a

slight increasing trend of occurrences of Fowl pox in ail the 5 districts of the

ing results, it appeared that Fowl pox occurred slightly in low levels in all the

studv and there was slight increasing trend of occurrences of Fowl pox in district

I pox is one of the oldest known viral disease of chickens, that has been eliminated

mmercial poultry farms in many parts of the world through use of the attenuated

r vaccine Since many poultry farms have discontinued the use of the vaccine in their

ly susceptible chicken population has consequently been appearing intermittently

il disappear

iiliiic literature Fowl pox is reported to be an acute contagious disease caused by HP

,ks of (iisease would affect the poultry industry in many countries (Biggs. I9S2).

i occurring through mechanical transmission by mosquitoes and mites A virulent

.is was isolated from a natural outbreaks of the disease in Sudan by GatVar ei a]

irus was used from experimental transmission of the disease to susceptible chickens

and intravenous methods were used to infect one-month-old chickens Scarification

al pox lesions at 5-7 days postinoculation, whereas intravenous injection induced

of combs or wattles, at 1 0-1 I days postinoculation, although neutralizing antibodies

pox virus were detected 2. .1 and 4 W'eeks postinoculation.The lesions of the disease

ed in the epidermis, the feather follicles, and in some cases the mucosa of the mouth.

pharynx, nasal chambers, larynx and trachea these findings fall in agreement with

by Biggs (1982). In the tracheal i.e diphtheritic form, white opaque nodules

lie mucous membranes, rapidly increasing in size and coalesce to form a yellow

125

re : 58

Trends of Fowl Poxon poultry farms of Karachi.

ZvJHi X

I/

/

72LHi

/

79 80 81 82 33 84 85 86 87 88 89 90 91 92

Years

-ÿ Data Smooth —ft— Regr

*.126

jure : 59

Trends of Fowl Poxon poultry farms of Hyderabad.

r\K 7t / \\ ! \

X? \ /ÿ

/

/27 V

JLi 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data — Smooth —**— Regr

12 7

ire : 60

Trends of Fowl Poxon poultry farms of Nawabshah.

7V H:

K Ij !

i \ \\

a—f—T”*

-Ai-

* i/7*

wV-f

V» --r

79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Smooth —1 RegrData

128

e : 61

Trends of Fowl Poxon poultry farms of Mirpurkhas.

i

A A--rtf¬'s—9*6-

/-/ÿ T

I

7/•••

I"/\

\

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79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

m

Data - Smooth — Regr

129v

e : 62

Trends of Fowl Poxon poultry farms of Sanghar.

n

>

-U

t

;

=*= ~4» --fr- j

79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data - Smooth - **- Regr.

130

imembrane has been reported by Richter-Reichhelm el a].. |0S5. The live infected

med for examination showed severe respiratory signs followed by suffocation

callv. the most important features are hyperplasia of the epithelium and

'f cells associated with inflammatory changes and characteristic eosinophilic

elusion bodies Bollinger bodies reported by fore going worker.

nilar report lias been published by (Beach. 1029) During natural infection, eruption

on various parts of body was suggestive of Fowl pox infection Extension of the

I the eyes lead to partial or complete closure of the eyes (Figure-57) In the

urn of the disease, lesions appeared in the mouth, esophagus and trachea

nlection in young chickens caused generalized lesions, poor feathering, and death

MI of laveis was reduced in the affected flocks

hy et. aj . ( 1074) made 2 isolations of Fowl pox virus from hens of an adult laving

iniversifv of Illinois poultry farm The birds from which isolations were made had

sions on the comb and wattle Periodic drops in egg production was also reported

; virulent for susceptible day-old chicks

dmg to the Tripathy el a] (1074). Fowl pox was only diagnosed from liens of an

lock in the university of Illinois poultry farm but lieie in this study Fowl pox was

all the commercial broiler and layer poultry farms throughout the Sindh province and

rate per farm of this disease as well as mortaiilv per fann was low 21 and i 1 ,l>'

1.11

*.

ons Bm.sal Disease (Guinboro Disease).

ns of Outbreaks.

ndv of patterns of outbreaks of Guinboro disease in !i\e districts of Sindh (Figure

lat the highest number of outbreaks w ere reported in Karachi 444 ( 2f) o av erage per

.1 bv Hyderabad i4S (9 S60 average per year). Nawabshah I4S (9 86b average per

khas I la (7 511 average per year) and Sanghar 90 (b average per year) with the

gliar Outbreaks of IBP were reported throughout the vear and the disease occulted

ng chickens.

lorlcm Lesions.

lorteni examination showed swollen bursa of Fabricius two or more times t he normal

di or hemorrhagic and contained a yellow cheesy material (Figure b4) Kidnevs

tv of changes, in some ctises normal and in others these were swollen Inlra-musculai

in breast, thigh and wing were also observed

lidity Rale.

e results (Table 4) showed that in Sindh I4S farms were affected with the disease and

1' this disease per farm was 406 !S4 (58,41 %) and the morbidity per farm was a 17 >9

tality Rate.

mortality rate of Guinboro disease per farm was I4S.790S (9.44 °-o) recorded trom

cial poultry farms of Sindh out of 3204 farms (Table 4)

e Fatality Rate.

results (Table 4) revealed that the Guinboro disease showed 21 5.1 percent case

from the above quoted numbei of farms

nds of Outbreaks.

rwise trend of occurrences of Guinboro disease in Karachi. Hyderabad. Nawabshah

. and Sanghar is summarized in Figures 65. 66, 67, 6S and 69. respectively. Except in

1 52

<juÿe : 53

imber of outbreaks of Guniboro disease

in Sindh

(breaks

y.'

IA 1

Districts

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.IPSwollen burea of Fabricius containing a yellow

cheesy material in Gumboro disease.

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Symptoms of Lymphoid Leucosis in adult chicken.

134

re : 65

Trends of Gumboro diseaseon poultry farms of Karachi.

1

7

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Ji 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Smooth RegrData

*>135

ire : 66

Trends of Gumboro diseaseon poultry farms of Hyderabad.

7

r_

*I

8 79 30 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data Smooth —: Regr!

136

ure : 67

Trends of Gumboro diseaseon poultry farms of Nawabshah.

i

77

z.rz

/

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:

8 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

h~ Data Smooth Regr

•x137

e : 68

Trends of Gumboro diseaseon poultry farms of Mirpurkhas.

-rr. ...

T*- .

Ii

Ht""

;

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79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data - Smooth — Regr

*.138

H*

ure : 69

Trends of Gumboro diseaseon poultry farms of Sanghar.

!I

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i/

V :

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“•

3 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

- Data - Smooth — Regr.

139

the disease showed a secular trend, tire regression line in other districts showed a

the disease

ling to literature review Infectious bursal disease (IBD) is a highlv contagious \ iral

ng domestic chickens throughout the world The causative agent of Gumboro

kens was first desciihcd be Cosgrove (1002), is double segmented, double-standeii

iclonging to the Birna virus familv ( Dobos et id., 070) Some of the clinical signs m

described bv Cosgrove (1002) included whitish orwatery diarrhea, anorexia.

I prostration Infection in voting chicks could result also in imnuinosuppiesvon

1072: Giambronc et ah. 1070) The primary target organ of IBD virus (IBDV) was

abricius. although Ivmphoid damage might occurred in the spleen, thymus and gland

veil (Cheville. 1067: Dohms et aj . 1 08 1 )

lions bursal disease (IBD) is of great economic significance m the poultry mdustrv

eld viruses can cause a highly contagious immunosuppressive disease that might

lections caused bv other etiologtc agents The disease which has the gieatest impact

ickens, typicalk produces lesions within the Ivniphoidal follicles of the bursa of

dlv el id . 1076) According to some workers Infectious bursal disease virus (IBDV)

>ative agent of a highly contagious disease of voting chickens (Gumboro disease)

; maiulv by severe changes in the bursa of Fabricius followed by immunosuppression

1072, Hirai et id , 1074, Fadly et id . 1076). it is well known that the virus persisted

iiment. and once the infection was established on a farm, it reoccurred in subsequent

r and Cho. 1965. Benton et a]., 1067. Edgar and Clio. 1075)

140

lioid Leukosis.

ns of Outbreaks.

from ihe data (Figure 70) that the highest number of outbreaks were reported in

(103 00 average per year) followed bv Mvderabad 520 (54.60 average per vear).

20 (54 no average per vear). Miipurkhns 405 (27 00 aveiagc per veai ) and Sangli.u

erage per yeai ). Lymphoid leukosis was reported throughout the vear and outbreaks

dull chickens. The lowest number of outbreaks were recorded in Sanghar

:e number of outbreaks of Lymphoid leukosis per vein in all the districts under stud\

The

lortcm Lesions.

toms of l.vmphoid leukosis observed during postmortem in adult chicken are shown

Lvmphoid Leukosis afTected chickens showed diffuse morbiditv officer (liguie ’’2)

.lily of liver (Figure 75). morbidity of kidnev (Figure 74). Fabliaus bursa (Figure "5)

igure 70) was observed

rbidity Kate.

results depicted in Fable 4 sluwved that, in Sindh. 520 farms were atVected with

and prevalence rate of this disease per farm was 220 S5 (60 S2 "n) and the

a farm was 154 S2 (20 56 %)

talitv Rate.

mortality rate of Lymphoid leukosis pet farm was 75 (IP 50 °o) recorded from 520

poultry farms of Sindh

c Fatality Rate.

t on case fatality rate are summarized in Table 4. These results revealed that the

eukosis showed 20.25 percent case fatality rate in 15 years of data recorded from 520

poult rv farms of Sindh.

141

*.

: 701 1 f-

linker oi oul breaks of Lymphoid Leukosisin Sindh

11•In

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142

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Diffuse morbidity of livei in Lymphoid leukosis.

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Mixed morbidity of liver in Lymphoid leukosis.

143

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Morbidity of kidney in Lymphoid leukosis.

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Morbidity of Fabricius bursa in Lymphoid leukosis.

14 H

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Morbidity of ovary in Lymphoid leukosis.

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Leg paralysis in classical Marek's disease.

145

lids of Outbreaks.

mvise trends of occurrences of Lvmplioid leukosis on commercial poultry farms of

vderabad. Nnwabshah. Mirpurkhas and Sanghar arc summati/.cd in figures 77. 7S.

respectively. The regression lines in these eases revealed a lising trend of the disease

lriels during I 5 veai s

mode of transmission of this disease has been discussed by many workeis I he

irciuls congenitally from dam to progenv or horizontally faun chicken to chicken in the

Studies bv Rubin and associates (Rubin et. _aj 1961 Rubin ei a| 1962) showed that

c infected chickens were imimmologically tolerant m that they failed to develop

al were permanently viremic These workers determined also, that a high percentage of

am imnumologicnlly tolerant hens were congenitally infected In contrast, chicken-*

horizontal transmission usually developed aiitibodv and congenital transmission from

vas often Itighlv erratic With the technology developed (Rubin et a] I960. Rubin ej

fubin e[ a] . 1962). it has been possible to develop docks of chickens lice of infection

uses (L.I.V) (Hughes et aj . 196.1. Zander ei aj . 1975) However, identifying hens that

lection erratically (Rubin. 1961. Calnek. 1965) is ditficult. the disease lias been

onlv from docks used largely for experimental purposes The chances of identifving

ire erratic in congenital transmission of infection has been greatlv increased bv the

hat eggs mav contain infectious virus in albumen prior to incubation even though

hitch develop subsequently in the same eggs may be negative for virus Even so. not all

ransmit infection could be detected by testing for vims in albumen because infected

ive been obtained from eggs that did not have infectious virus in albumen (Spencer et

In light of these lindings it is necessary to distinguish between congenital transmission

ng of virus The term congenital transmission was used here by some workers to

ection of the embryo with virus derived from the dam. whereas shedding of virus

he release of vims fr om cells of the dam into the egg albumen In addition to shedding

) hens also shed group-specific (gs) antigen into egg albumen. The gs antigen was

to an internal structural component of the vims that was common to viruses of the

coma group (Bauer and Schafer. 1966. Purchase and Burmcster, 1972).

*

! 46

•v

7*

lure : 77

Trends of Lymphoid Leukosison poultry farms of Karachi.

i

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'• -ZKTi

\ z5—I--— +77 4*'

T T T T T T r T r r$ 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

—1 Data Smooth — Regr+

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Trends of Lymphoid Leukosison poultry farms of Hyderabad.

j

\

\\

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TT .\

*ÿ. -77\

Tt-'-/

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* 1

TT Tr T

78 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data S.nooth — Regr

140

J

5

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Trends of Lymphoid Leukosison poultry farms of Nawabshah.

;

j

/ \i

I.\ I

+

*/x

V-K:

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T T T T T r r T

; 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data — Smooth — Regr

149

i

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Trends of Lymphoid Leukosison poultry farms of Mirpurkhas.

w

I

••••»*•>7

\

\

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* I/

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5 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data Smooth — Regr+

150

•i

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jure : 81

Trends of Lymphoid Leukosison poultry farms of Sanghar.

i

I

7T

,/ i -+ +I y

i\

' \I

m\_„*r' :

i\

jt..*r

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*Tr-fT T T T T 7 T [

’8 79 80 81 82 83 84 85 36 87 88 89 90 91 92

Years

— Smooth — Regr.Data

151

V

mphnid leukosis viruses (LLV) are found in most commercial poultiy flocks, and most

i a (lock are exposed to infections, and to most vims at some time during their life time

m infected chicken eventually develop lymphoid leukosis (II.) depends on a \aiietv of

ices: aye of exposure level of exposure, genetic susceptibility, of the stiam of chicken

latemal nntibodv and other important factors still undefined J.vmphoid leukosis (Li t in

x a malignancy of lymphoid tissue dependent on the bursa of inbiunits In present stud'..

leukosis xs as reported from many of the commercial poultiy farms of Sindh though the

per farm was low (20 .>6 °o). and mortality per farm was also low ( 10 16 nn). according

tistical analysis of data the disease showed a rising trend The othoi workers haw also

o\v and sporadic occurrences of this disease According to Purchase and Burmestei

totialiiy from this disease occurs only sporadically in most poultry (locks, suhclimcal

with the causative virus aic widespread and probable occui in all commercial poultrx

1 52

.•k’s Disease.

•ras of Outbreaks.

> pears from Figure 82. that the greater number of outbreaks !ia\ e occurred in Karachi

tverage per year) followed bv Hyderabad 504 (20 (>0 average per year). \awab.4uh

tverage per year). Mupuiklias 214 (14 20 average per year) and Sanghar 1 74 ( 1 I

year) Outbreaks of Ml) were reported throughout the year and most commonK the

treed in between 4 and 24 weeks of age The overall av erage number of outbreaks of

iei vear was 128 5a

hi

Imot tem Lesions.

tv birds brought from the Marek’s disease affected docks for postmortem examination

r ptualvsis (l-'iyure 85). wing paralysis (figure 84). paralvsis of the legs and neck

and other s\mptoms of acute Maiek's disease (figure 88) Morbidity of the sciatic

re So), moibidilv ol ovarv (figure 87) were eommonlv observed during postmortem

i m classical March's disease Morbidity of viscera I figure 84). morbiditv of live!

moihiditv of heart (Figure 4]). morbidity of lung (Figmc 42) and morbiditv of skill

were also observed in acute cases

rhidity Rate.

results for morbiditv rate of Maiek's disease arc presented in fable 4 These results

.1 504 farms were affected with the disease and it's prevalence per farm was 27o "4

uul the morbiditv per farm was 140 IS4 (25 50 °n)

rtality Rate.

mortality Kite of March's disease per farm was S5 S6 (12.25 no) recorded from 5t °1 poultrv farms of Sindh (Tabled)

<e fatality Rate.

44 percent case fatality rate was calculated from the data spread over 1 8 years

out 504 commercial pnultrv farms of Sindh (Table 4)

I 55

"s

Figure : 82

Number of outbreaks of Marek's disease

in Sindh

u>ilbreaksI ODD

f!U()

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in;ÿr*U

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Wing paralysis in classical Ma r e k1

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classicalParalysis of the legs and neck in

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Morbidity ot sciatic nerve in classical Marek’s disease.

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Morbidity of ovary in classical Marek's disease.

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Morbidity of lurwj in acute Marek's disease.

m-)y

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Morbidity of skin in acute Marek's disease.

159

of Outbreaks.

of occurrences of Marek's disease on commercial poultry farms of Karachi.

.vabshah. Mirpurkbas and Sanghar are summarized in Figures 04. 05. 0<>. 07 and

The regression lines in these cases revealed a rising trend of the disease

disease (MD) is a highly contagious neoplastic disease of domestic chickens

pesvirus (MDY). The pathological changes of MD are characterized by lymphoma

\iscera and lesions in the peripheral nerves It is well known that MDY infection

long period and that some infected chickens actually develop clinical MD Some

igations proved that the incidence of MD was correlated with virus multiplication

he initial stage after infection and also with persistence of infection (Witter et aj

ill - 1972. Sleek and Maharslieh. 1076. Fabricant et a] . 1077) Since the scale of

listrv is increasing, the use of a reliable vaccine to prevent outbreak's of MD m

. becoming very important In earlier studies the turkey herpesvirus (MYT) vaccine

d to be higltlv effective m reducing the mortality of chickens from MD (Okazaki et

tase et al . 1072) However, MD is still one of the major causes of poultry losses in

irious countries of the w orkl. even in the presence of vaccine (Okazaki el ai . 1 07.T

'ÿ>. F.idson et id . IOS I )

!. Payne and Rennie (1972) reviewed the pathogenesis of Marek's disease (MD)

npublished observations, later detailed (Payne et al • 1076). forming the basis for a

ich appeared fundamentally correct. Briefly, he and Rennie found that neonatal

•oupled with sublethal X - irradiation, increased the incidence of lymphomas in

stant chickens subsequently exposed to Marek's disease virus (MDY). but had the

t with genetically susceptible chicks. They concluded that the thymus was the

teoplasticallv transformed cells composing one component of MD Lymphomas and

hymns - dependent immune system was signiticant in surveillance and control of

mnl information gathered from several laboratories made it abundantly clear that

1 indeed had such a dual role in MD Neoplastically transformed cells have been

-cells, largely on the basis of studies with lvmphoblastoid cell lines (Nazerian el al .

160

gure : 94

Trends of Marek’s diseaseon poultry farms of Karachi.

\KV.U-X.

\

\/V i .M

\/ .

V78 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Smooth — Regr— Data

161

r

<

jre : 95

Trends of Marek’s diseaseon poultry farms of Hyderabad.

m

/A j

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—tr\ V

.

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/7

8 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

- Data Smooth — Regr

162

lure : 96

Trends of Marek’s diseaseon poultry farms of Nawabshah.

1

Ax n\ i

:—* /\\/

1

\\ :1

2- ii x

u ¥y

8 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

- SmoothData *— Regr

163

f

ure : 97

Trends of Marek’s diseaseon poultry farms of Mirpurkhas.

/

/ \V.

JJL.-s+r

\

A ' >'T"\«

/i- /

\j/jV

79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years<

— Smooth —: RegrData

V164

re : 98

Trends of Marek’s diseaseon poultry farms of Sanghar.

i\r \

-TK—)

A-t#- Nv \

\JL\ T\

i\

m/ i

\//M

3 79 80 81 82 83 84 85 86 87 88 89 90 91 92

< Years

Data Smooth — Regr.;

165

n

well et a] . 1074; Mutsuda el a]., 1076) Impairment of the thymus, but not

undent immune system has generally resulted in atleast partial abrogation of the

they have come to associate with immunological competence in chickens (Sharma et.

Sharma and Witter. 1075)

166

I

i* Disease.

uf Outbreaks.

: ns of outIncal\ s of \ow castle disease ( \ I) i in live disl:ka< . >f siiulii ,IK' dop'dcu

•ii 'hem data n ou:U1 iv H'i’ii « h:si hiehe-t numbei ' V. Cl l- I Opt •: Vv3 "

(’H aveiaoc |Vi \cai> foi'ouc.i 'w 1 |\ dci ;:Kk! MM- ( ~d aveiaoc pci \Aii 1

\ IIIPill kiUlN

' aveiaoc per voaii ( >i r.hi c.ik . f \l) -.'.is 'opened tm eiionoul the vcai .in.!

I'ho evciall avcinne number outbi oak-' of ’iv

•!ÿ' .octane poi vo.ii I I1•" - .iv o:.loo poi V OJI I dV

s

1 1 od in 11)0 buds of ill aces

.('ÿ i ;>

cm l.o ions.

sulnov s IIKI homoi i banes in ihe pnov cull 'coins 1 1 m n ; 1 > vv oi o ol'>oi \ cJ :i'.o

chickens. Iiouie M'l .inJ M1?. showmn mis->hnpcd ov ,n ION of \cw castle disc.PC

A! pow eiiiriailus showed verv marked and clinrac!-.-: sn. kcmeirhaoic lesions

-ii'iis caused by ihi.s disease could alVcoi ilie ocninil no'v.'us w stem icspnaier.

loins Mans In.o hild.s bronchi liom ihodisoaso atVcclod ll.vks showed complete

ofiho wines and loos il-'inine MM) I lemon banes in ihe now oninouliis of the

olnokon (I'lL'UK i‘ ) was nlwoivod fici|iienlK in mo-t in' ilio hnds dunno

lunation The oilier (Moans show inn ilie svmpionis of i lie disoaso observed in die

no demonstrated in I’ueure l"o shows respiiateiv svniptoms heme 1"“

'inure InS spleen and l-iyuic l()° lal lissuo. 1'iniiic 1 lo wind-pipe of \|) (the left

idinoss nf nuiomis memhiano and llie increased mucus, and the noli! showed

leedinn) Morhiditv ofovary m the disease was also ohsoivod 1 1 ionic III) Blood

lonhanc in the proveniiiuilus and small intestine wore ohseivecf m Velpecmc

cwoasilo disease (l-inure lid) I iome II.’ shows lame miestine of \ \ \I>

will) blood pat olios and linm e I It show s blood patches and ncerosi of the eeea!

od ease ol \ V\'D l:\cessi\e lluids weie 11 e(|iiemK seen in the respnaloiv tract

isceioliopic \'ewca -lie disease dm inn postmortem examination ilinme IIM

a! edema ol' the evclids in VV\D (I’iemc IlM) were cninnionlv observed

I f'7

I

: y'i-cf.i|«*

Number of oufbrcnks of Newcastle Diseasein Sindh

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nucous men or one end increased mucus, and the

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174

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Newcastle disease ( WND) ,

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177

ge m t he mucosa of the trachea in a VVND affected chicken (Figure I 17) was also

n some cases during postmortem examination

orhiditv Rate.

e results lot morbidity rate of New castle disease (ND) are presented in Table 4 In all

is were affected during different periods with Newcastle disease and prevalence rate of

se per farm calculated was .»S(> 5 1 (65 95nn) and the morbidity rate was 26n 4S

Oi't:ilit \ Rate.

ie mortality rate of Newcastle disease per (arm was 260 48 (24 75 00) recorded from

inercia! |ioultty farms of Sindh (Table 4)

lsc I'nlalilv Rate.

ie results showed 54 ol percent case fatality rate from I0S7 commercial poult IA farm

)4 farms of Sindh (Table 4)

ends of Out breaks.

ends of occiinences of the disease on commercial poultrv fauns of Kaincht. Hyderabad.

ill. Mirpurkhas and Sanghar are depicted by Figures 118. Iff). 120. 121 and 122.

The regression lines showed rising trend of the disease in these districts

ewcastle disease (ND) outbreaks are still common, even though mass immunization

D is practiced throughout the commercial poultry industry of the province The affects

an range from no svmpioins or mild nirsacculitis to severe nervous and or visceral

mt leading to paralysis and death Broiler chickens are vaccinated against ND

ally by several routes drinking water, intraocular, inuanasal. intratracheal, and aerosol

a] . 1975. Eidson e_r a] . 1976; Eidson and Kleven. 1976) The age at vaccination and the

maternal antibody greatly influence the hemagglutination-inhibition (III) response of

ickens (Allan. 1975, Kleven et a] . 1975; Eidson et al . 19S2) There has been a concern

viler industry that ND vaccines from commercial manufacture may not he inducing a

t antibody response in the broiler chicken

I7S

rjure : 118

Trends of Newcastle diseaseon poultry farms of Karachi.

|TI

/ÿ j

\ x7/ v L -~h :

:__

rr\w-i

7V-

j

’8 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data - Smooth Regr

179

f

Figure : 119

Trends of Newcastle diseaseon poultry farms of Hyderabad.

180

£160

140

L\120

/ \to

% 100 31-0)

n /5 80 zxo JL60L

40

20

078 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

- Data Smooth Regr

:

f180

Figure : 120

Trends of Newcastle diseaseon poultry farms of Nawabshah.

180-

160

140

I120-w

1008x5

A803o

60 / r /.,40---H-;

20

078 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

- Data Smooth —**— Regr

I

181

Figure : 121

Trends of Newcastle diseaseon poultry farms of Mirpurkhas.

120

100-

80'<s>

iS60-

23o

40-

20- m

0 -m m78 79 80 81 82 83 84 85 86 87 38 89 90 91 92

Years

Data Smooth — Regr

1D2

i

Figure : 122

Trends of Newcastle diseaseon poultry farms of Sanghar.

1407—

L120

1C0

Iw

a 80 -K-

2/ i\t£ 60

ZvO

40

stf"

20 70

78 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

E Data - Smooth —*«— Regr.

183

Newcastle disease vims (NDV) strains differ in pathogenicity in chickens . different strains

nodiice clinical conditions that range from a severe respiratory, neurologic, or enteric disease and

tenth to an asymptomatic infection. Rapid differentiation of virulent and avirulem strains is

imperative in order to rapidly initiate appropriate control measures. Foi a long time, assessing

irulence of isolates has been based on pathotyping procedures that include mean death time ot

pathogenicity for chickens, and plaquing characteristics in chicken embryo fibroblasts

Beard and Hanson, 1084). In the present studv too the affected birds with different clinical

-ondilions were produced for postmortem.

Since the last epornitic of Newcastle disease virus (NDV) of the late 1060s to 1070s. the

lisease has persisted in the Middle Hast in endemic form. Periodic isolation and typing of

elogenic field strains have revealed the prevalence of isolates of moderate virulence and the

iccasional occurrence of highlv virulent strains similar to VLT 68. VAIB 74. and B75 isolated

ictween IOCS and 1075 (Zein. 1074: Singh el a] . 1078) This report described the biological

properties of an isolate from Saudi Arabia, SAS4 A few months following the isolation of SAS4.

i severe epornitic invaded Lebanon; an isolate from a broiler flock. SML85. had the major

•haracteristics of SAS4. but it differed in plaque morphology and virulence. Looking at the

presently rising trend of this disease in the province it becomes imperative to cany on work on

yping of strains as well

Newcastle disease vims (NDV) has been known to produce conjunctivitis, blepharitis, and

orneal and lens opacities in chickens infected naturally or experimentally (Clark ei al . 1955.

fheville and Beard. 1972; Katoh, 1977). It has been proposed, but not established, that the

pathogenesis of the ocular and periocular regions are of systems in origin (Clark el al.. 1955.

Dradiri ei a] . 1959, Pannu and Bankovvski, 1962; Bankowski et al., 1963), virus has been

iemonstrated in the aqueous humor of chickens infected with NDV (Dradiri et al., 1959, Pannu

md Bankowski. 1962, Cheville and Beard, 1972), and some authors have suggested that the virus

eaches the aqueous humor through the ciliary body (Spalatin et al , 1973) Other avian v iral

nlections, including avian encephalomyelitis and Marek’s disease, have been shown to invade the

ye during systemic spread (Flowers et a]., I95S).

1S4

In the present study Newcastle disease was reported from most of the commercial broiler

and layer poultry' farms of Sindh and the morbidity rate per farm of this disease was 24 75

percent, the mortality per farm was aiso 24.75 percent and according to ihe statistical analysis

data on occurrence of Newcastle disease showed a rising trend in Sindh inspite of vaccinations of

the flocks This is a high morbidity and high mortality disease.

185

If

I

4.5.6. Angara Disease (Hydropericardium Syndrome).J.

(a) Patterns of Outbreaks.

The patterns of outbreaks of Angara disease in five districts of Sindh are depicted in

Figure 12.1 From these data, it appears that the highest number of outbreaks were reported in

Karachi 669 (44 60 av erage per vear) followed bv I Ivderabnd 221 (14 SO average per vean.

\awabshah also 221 (14 S6 average per year). Mirpurkhas 170 (li 71 average pei vear) and

Sanghar I >9 (9 20 average per year) Outbreaks of Angara disease were recorded throughout the

vear and the disease mainly occurred in broileis and rarely in layers The lowest number of

outbreaks were reported in Sanghar and the average number of outbreaks of Hydropericaidium

per year on pooled data from all the districts was 95.11

Postmortem Lesions.(b)

During postmortem examination of the affected birds, most conspicuous feature of the

disease is of presence of fluid in the pericardium. Mvdropericardium (Angara disease) cases

contained 5 ml to 15 ml. fluid with some hemorrhages on the heart as characteristic lesions of

Hydropericaidium Enteritis, necrosis on the spleen, hepatitis with hemorrhages on the liver.

nephritis, dehydration of muscles and enlarged bursa with yellowish material were also the

characteristic lesions of the disease observed during postmortem examination m this studv in the

laboratoi ics.

(c) [Morbidity Rate.

The data summarized in Table 4 showed that in Sindh 221 farms were affected with

Hydropericardium and prevalence rate of this disease per farm was 221 28 (69 26 To) and the

morbidity rate per farm was I 54.17 (II 54 %)

(d) Mortality Rate.

The data shown in Table 4 revealed that the mortality rate of I lydropcricardium per farm

was 68 9 1 (5. 17 %) reported by 221 commercial poultry farms of Sindh.

1S6

ir

Figure : 123

Number of outbreaks of Hydropericardiumin Sindh

outbreak’s700

000

r»oo

401)

300

m200

illm100

l.m\W\ t0

Districts

1

__] NnrrnliSlinliK?9 Kai.-ulii

Wffh MirpiirhIms

t\\\\v3 Hyderabad

Snnghar

(1978- J 01)2)

187

(c) Case Fatality Rate.

Table 4 also revealed that the Angara disease showed 12.72 percent case fatality rate on

the pooled data from the year 1 087 to 1992 recorded from 22a commercial poult rv farms of

Sindh.

Trends of Outbreaks.(0

Trends of (recurrence of Angara disease in poultry farms of Karachi are presented in

Figure I 24 The regression line showed rising trend

Yearwise trends of occurrences of Angara disease (Hydropericardium Syndrome) in

Karachi. Hyderabad. Nawabshah. Mirpurkhas and Sanghar are depicted in Figures 124. 125. 126.

showed a rising trend of the disease in these127 and 12S. respectively. The regression lines

districts.

.Angara disease was firstly reported in July, 1987 at Meraj poultry farm and Mushaiuf

poultry farm at Angara village Karachi Immediately after three months, the disease was reported

in many of the poultry farms in Karachi and then lesions of this disease were reported throughout

the country and were specially diagnosed in live districts of Sindh province included in tins study

The disease was mainly reported in broilers and rarely in layers. Since. I9S7 the research on its

causes has been initiated The review' of scientific literature revealed a few reports

The clinical, hematological, biochemical and pathological changes were described bv

Jantosovic et a].. (1991) in 5 outbreaks of the disease. Another study was carried out by Afzal el

a], (1991) to determine the etiological agent (s) associated with hydropericardium (Angara

disease) in broilers in Pakistan The results indicated that in addition to adenovirus some other

agent was involved in causing the disease, but that this agent required co-infection by an

adenovirus for the reproduction of the typical signs of the syndrome The nature of this agent

remained unknown because no discrete virus or virus-like particle could be seen by electron

microscopy. So far, the present study is concerned, Hydropericardium (Angara disease) was

diagnosed in poultry disease diagnostic laboratory on the basis of postmortem examination and

the lesions are described.

188

Figure : 124

Trends of Hydropericardiumon poultry farms of Karachi.

250

200

\150

to

<3

- 100-X)

O50

0 m

-50 T

78 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Smooth — Regr- Data +

189

r

Figureÿ : 125

Trends of Hydropericardiumon poultry farms of Hyderabad.

80

70

X60 ¥

50

n 40-31)

30

/D—J

J 2070

10

0

-10*T'

-2078 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data Smooth - Regr+

190

Figure : 126

Trends of Hydropericardiumon poultry farms of Nawabshah.

80

70V

k60

50

CO 40co0)

30A

13 20O

10

0

-10

-20 TT

78 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Smooth —: RegrData

191

?!

Figure : 127

Trends of Hydropericardiumon poultry farms of Mirpurkhas.

70

601

50-

40-)

30i

! 20-i)

10-

0 m m m

-10i

-20 rT T T T T T T T T T T T T

78 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data Smooth — Regr+

>192

Figure : 128

Trends of Hydropericardiumon poultry farms of Sanghar.

60

50

40

OT 30(0CD

20.Q

DO 10

0

-10

-20 T TT T T T T T T T Tr T r

78 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Smooth Regr.l— Data +

193

fi

4.6. PARASITIC DISEASES.

4.6.1. Coccidiosis.

(a) Patterns of Outbreaks.

The patterns of outbreaks of Coccidiosis in five districts of Sindh are depicted in Figure

129. Outbreaks of Coccidiosis were recorded throughout the year and the disease was mainly

reported from young chicks and growing stock. It appears from the data that the highest number

of outbreaks were reported in Karachi 364S (243.2 average per year) followed by Hyderabad

1216 (SI.066 average per year). Navvabshah 1216 (81.066 average per year). Mirpurkhas 1055

(70.333 average per year) and Sanghar S75 (5S.333 average per year).

(b) Postmortem Lesions.

Figure 130 shows small intestine of chronic form of Coccidiosis and Figure 131 showed

blood in small intestine and large intestine with characteristic swelling observed in postmortem

examination. Swollen caeca filled with a bloody mass (Figure 132) were found to be the

characteristic lesion of caecal coccidiosis. Hemorrhage on the caecal tonsils, small intestine and

other organs (Figure 133) were also observed in caecal Coccidiosis and Figure 134 showed caeca

of a pullet distended with blood in E.tenella Coccidiosis During last stage of E.tenella infection.

caeca contained pink and white cores, formed from blood cells, plasma, tissue debris (Figure 135)

When the E.tenella caeca were opened, a bloody mass was revealed, as a result of blood vessels

hemorrhaging in the organ (Figure 136). The caeca were observed swollen and were filled with a

bloody mass containing lymph, tissue cells and other debris (Figure 137) observed on postmortem

conducted in the beginning stage of Eimeria tenella Coccidiosis. Characteristic swelling of the

small intestine were noted (Figure 138) in E.necatrix Coccidiosis. The intestine was ballooned or

severely swollen. Hemorrhagic areas were seen outside the organ and the caeca were usually filled

with blood from the intestine in Eimeria necatrix Coccidiosis too (Figure 139). In some cases a

portion of upper half of intestine showed whitish patches (Figure 140) which might be result of a

light infection, these lesions were seen from outer side of intestine as well as on the inside in

Eimeria acervulina Coccidiosis and in a heavy E.acervulina infection, lining of the intestine was

observed bright red in postmortem examination (Figure 141).

194

y

!

Figure : 129

Number of outbreaksof Coccidiosis in Sindh

Outbreaks4000

3000

2000

1000

Districts

Figure

Hyderabad

feilH] Sanghar

E8& Karachi

Mirpur Khan

I _ 1 Nawab Shah

(1978 - 1992)

195

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Small intestine lesions in chronic Coc cicliosis.

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Hemorrhage on the caecal tonsils, small intestine

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Caeca of a pullet distended with blood inE.tenella Coccidiosis.

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SS&i:Last stage of E.tenella infection. Caeca contains

pink and white cores, formed from blood cells,Plasma, tissue debris.

.

198

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vessels hemorrhaging in the organ.

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Characteristic swelling of small intestine

in E.necatrix Coccidiosis.

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Severely swollen intestine filled with bloodin E.necatrix Coccidiosis.

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infection in E.acervulina Coccidiosis.

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MLining of the intestine being bright red in a heavy

E.acervulina Coccidiosis.

•201

T:

(c) Morbidity Rate.

The results for morbidity rate of coccidiosis are presented in Table 4. The results showed

that in all 1216 farms were affected with coccidiosis and prevalence of this disease per farm was

406.95 (72.46 %) and the morbidity per farm was 278.92 (32.55 %).

(d) Mortality Rate.

The mortality rate of Coccidiosis per farm was 128.0366 (14.18 %) recorded from 1216

commercial poultry farms of Sindh out of 3204 farms (Table 4).

(c) Case Fatality Rate.

The results revealed 22.94 percent case fatality rates on analysis of data for 15 years from

1216 commercial poultry' farms of Sindh (Table 4).

(0 Trends of Outbreaks.

Trends of occurrences of Coccidiosis on commercial poultry farms of Karachi. Hyderabad.

Nnwabshah, Mirpurkhas and Sanghar was observed in Figures 142. 143. 144. 145 and 146.

respectively. The regression lines showed rising trend of the disease in these districts

The increasing trends of outbreaks of Coccidiosis revealed unsatisfactory management and

disease preventive measures adopted by the poultry farmers.

fReid (1990) reported that fifty years ago, Coccidiosis was probably the most feared

disease of advanced poultry producers of that day. Because of the discovery and use of preventive

chemotherapy, that fear is no longer. However, improving methods for controlling these

protozoan parasites remains high on priority lists requesting new' research from the poultry

industry. Severe mortality losses have become less frequent, but decreased production efficiency

continues to produce morbidity losses due to coccidial infections. The industry has found that use

of an anticoccidial drug is generally cost-effective as insurance against losses. However, the

recurring expenditure for required medication in large scale poultry production reminds producers

that control of this disease will be a continuing expense unless some cheaper methods of control

are discovered. Among the parasitic diseases of poultry the Coccidiosis is a cause of great

:oncern in our poultry industry.

:

202

Figure : 142

Trends of Coccidiosison Poultry farms of Karachi.

800

700

600

500

400

fr300-

_ M, _ —*—*£ / 7200V

100 M ¥o78 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data Smooth Regr

203

I

Figure : 143

Trends of Coccidiosison poultry farms of Hyderabad.

250

200

$ 150

<B

£a 100

50

078 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

RegrData Smooth

204

figure : 144

Trends of Coccidiosison poultry farms of Nawabshah.

250

200

£ 150Q)

a§ 100

50

078 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data Smooth Regr

205

Figure : 145

Trends of Coccidiosison poultry farms of Mirpurkhas.

250

200-

J2 150-

n

o 100'

350-

078 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data Smooth Regr

206

r

Figure : 146

Trends of Coccidiosison poultry farms of Sanghar.

250

200

" 1508Q

0 100

50

0—1-I-I-1-I-1-I-I-1-1-1-1-I-,-r-78 79 80 81 82 83 84 85 86 87 88 89 90 91 92

Years

Data Smooth Regr.

207

F

TABLE-5 ANALYSIS OF VARIANCE OF DATA ON OUTBREAKS OF V ARIOUSDISEASES IN KARACHI.

/

Source of variance Degree of freedom Sum of square Mean of square F. Ratio

2727904.42 32734S53 04 1.48 N SDisease 12

1 570457 1 1 21986399 54 0.14 N.SYears 14

9 1SS76.45 154371243.6168Error

194

TABLE-6 ANALYSIS OF V ARIANCE OF DATA ON OUTBREAKS OF V ARIOUSDISEASES IN HYDERABAD.

Source of variance Degree of freedom Sum of square Mean of square F. Ratio

Disease 12.15 S345035.3612 4140424.04

Years 0.009 N.S14 340695.8824335.42

Error 168 205055.14 34449263.52

194

208

*

TABLE-7 ANALYSIS OF VARIANCE OF DATA ON OUTBREAKS OF VARIOUS

DISEASES IN NAWABSHAH.

Source of variance Degree of freedom Sum of square Mean of square F. Ratio

Disease .145035 3612 4140424 04 12.15 S

Years 24335 42 340695.8814 0.009 N S

205055 14Error 168 34449263 52

194

TABLE-8 ANALYSIS OF V ARIANCE OF DATA ON OUTBREAKS OF VARIOUSDISEASES IN MIRPURKHAS.

Source of variance Degree of freedom Sum of square Mean of square F. Ratio

Disease 12 336746.88 4040962.56 1 88 N.S

Years 14 153309.47 2146332.58 0.09 N.S

Error 16S 131832.39 2214784 1.52

194

209

f

TABLE-9 ANALYSIS OF VARIANCE OF DATA ON OUTBREAKS OF VARIQUSDISEASES IN SANGHAR. i

Source of variance Degree of freedom Sum of square Mean of square F. Ratio

Disease 278318.612 3339823,2 3.01 N S

78994.3Years 1 105920,2 0.09 N S14

711 1 1.82Error 168 I 1946785.76

194

TABLE-10 MORBIDITY AND RANKING OF THE DISEASES ACCORDING TOTHEIR IMPORTANCE AND RESEARCH PRIORITY.

Morbidity (%)Disease Importance Research Priority

CoccidiosisMarek's DiseaseNewcastle DiseaseCRDFowl PoxInfectious Coryza

Lymphoid LeukosisFowl CholeraGumboro DiseaseSalmonellosisCoiisepticaemiaAngara DiseaseFowl Typhoid

32.55

25.3024 75

23.99521.0620.67

20.36

20. 16

19.7415.788

1 1.85

5I

82

2

64

5 7

96

7 10

I I8

I9

310

12

I 1.54 12 4

9.70 1313

210

- .y*

In the present study Coccidiosis has been diagnosed in all the poultry farms of Sindh and

the morbidity rate per farm of this disease was 32.55 percent, the mortality per farm was low

(14. IS %) yet due to unhygienic conditions the disease poses a constant threat. Many varieties of

coccidiostatic drugs are available for use as feed additives for controlling the Coccidiosis in

chickens; but inspite of that, according to our data on occurrences of the disease showed a rising

trend in the province during the period of study and this disease is continually creating problems

in modern poultry industry, reason may be still the same as reported by Reid ( 1990).

Analysis of variance of data on outbreaks of various diseases presented in Table 5. Table

8, and Table 9 respectively showed non-significant difference amongst diseases and years in

Karachi, Mirpurkhas and Sanghar districts and analysis of variance of data in Hyderabad and

Nawabshah (Table 6 and Table 7) showed significant variance amongst diseases and

non-significant variance amongst years.

The different diseases investigated in the present study are assigned importance according

to their prevalence rate in the province, the diseases are also assigned the research priorities

(Table 10).

211

1v

Ti

CHAPTER- V

SUMMARY

The data on poultry diseases from 1978 to 1992 was obtained from Karachi, Hyderabad,

Nawabshah, Mirpurkhas and Sanghar which are rich in commercial poultry farms and poultry

disease diagnostic laboratories are also working in these districts and besides collection of the

data, the diseased birds suffering from different bacterial, viral and parasitic diseases brought from

different commercial poultry farms were diagnosed in these laboratories on the basis of

postmortem examination and serological tests. Six bacterial diseases i.e. Salmonellosis, Chronic

respiratory disease, Colisepticaemia, Fowl cholera. Infectious coryza and Fowl typhoid, six viral

diseases i.e. Fowl pox. Infectious bursal disease, Lymphoid leukosis. Marek’s disease, Newcastle

disease and Angara disease (Hydropericardium Syndrome) and one parasitic disease i e

Coccidiosis was diagnosed in this study.

The data on the educational level and age structure of the poultry' farmers was collected in

order to assess the interest of people of different age groups in poultry farming, it was observed

that in the province 2.5% poultry' farmers were non-matriculate, 38.2% matriculate, 7.4%

intermediate. 29.3% graduate and 22.4% un-educated. 10.9% farmers were 18 to 20 years.

15 7% 21 to 25 years, 19.8% 26 to 30 years, 22.3% 31 to 40 years and 31.3% people involved in

poultry business were in between 4 1 to 50 years or above.

The data was statistically analyzed to study the patterns and trends of poultry diseases, the

results revealed that out of 3204 commercial poultry farms I32S farms u'ere affected with

Salmonellosis and the highest number of outbreaks were reported from Karachi (261.333 average

per year) followed by Flyderabad (88.533 average per year), Nawabshah (88.533 average per

year), Mirpurkhas (75.2 average per year) and Sanghar (60.133 average per year). The lowest

number of outbreaks were recorded from Sanghar. For Salmonellosis morbidity rate per farm w as

15.78S%, mortality rate 8.274% and case fatality rate averaged 14.763%.

212

x

CRD affected 636 farms with highest in Karachi (127.266 average per year) followed by

Hyderabad (42.4), Nawabshah (42.4), Mirpurkhas (33.266) and Sanghar (27 ). The morbidity

rate, mortality rate and case fatality rate averaged 23.99%, 1 1. IS% and IS.89% respectively.

Colisepticaemia affected 470 farms with highesl in Karachi (94. average per year)

followed by Hyderabad (31.333). Nawabshah (31.333). Mirpurkhas (26 07) and Sanghar district

(22.67). The morbidity rate, mortality rate and case fatality rate averaged 1 1.85%, 5.25% and

12.84% respectively

Fowl cholera affected 81 farms with highest in Karachi (16 2 average per year) followed

by Hyderabad (5.4), Nawabshah (5.4), Mirpurkhas (3.533) and Sanghar (2.4). The morbidity rate.

mortality rate and case fatality rate averaged 20. 16%, 9. 14% and 23.47% respectively.

Infectious coryza was reported from 463 farms and the highest number of outbreaks were

reported from Karachi (93.2 average per year) followed by Hyderabad (30.S66), Nawabshah

(30.S66), Mirpurkhas (23.733) and Sanghar (18.2). The morbidity rate, mortality rate and case

fatality rale averaged 20.67%, 10% and 15 625% respectively

Fowl typhoid affected 4 I farms with highest in Karachi (8.2 average per year) followed by

Hyderabad (2.733), Nawabshah (2.733), Mirpurkhas (1.066) and Sanghar (0.4). The morbidity

rate, mortality rate and case fatality rate averaged 9.70%, 7.40% and 25.08%.respectivelv.

Fowl pox affected 55 farms with highest in Sanghar ( 1 1.666 average per year) followed by

Karachi (10.6), Hyderabad (3.666) and Nawabshah (3.666). Outbreaks reported from Mirpurkhas

were (0.733 average per year) and it was observed that the lowest number of outbreaks were

recorded from Mirpurkhas. The morbidity rate, mortality rate and case fatality rate averaged

2 1.06%, 1 0.97% and 22.225% respectively.

Infectious bursal disease affected 148 farms with highest in Karachi (29.6 average per

year) followed by Hyderabad (9.866). Nawabshah (9.866), Mirpurkhas (7.533) and Sanghar (6 ),

The morbidity rate, mortality rate and case fatality rate averaged 19.74%, 9.44% and 21 53%

respectively.

Lymphoid leukosis affected 520 farms with highest in Karachi (103.66 average per year)

followed by Hyderabad (34.66), Nawabshah (34.66), Mirpurkhas (27.) and Sanghar (IS.53 ). The

213

morbidity rate, mortality rate and case fatality rate averaged 20.36%, 10.36% and 20.23%

respectively.

Marek's disease affected 300 farms with highest in Karachi (61.46 average per year)

followed bv Hyderabad (20.60). Nawabshah (20 60). Mirpurkhas (14.26) and Sanghar (I I 60)

The morbidity rate, mortality rate and case fatality rate averaged 25.308%, 12.254% and 23.49%

respectively.

Newcastle disease affected 1087 farms with highest in Karachi (216. average per year)

followed by Hyderabad (72.46), Nawabshah (72.46), Mirpurkhas (60.40) and Sanghar (4S S6)

The morbidity rate, mortality rate and case fatality rate averaged 24.75%, 24 75% and 34 61%

respectively.

Angara disease was reported from 223 farms with highest in Karachi (44.60 average per

year) followed by Hyderabad (14.86). Nawabshah (14.86), Mirpurkhas (11.73) and Sanghar

(9.26). The morbidity rate, mortality rate and case fatality rate averaged 11.54%. 5 17% and

12.72% respectively.

Coccidiosis affected 1216 farms with highest in Karachi (243.2 average per year) follow ed

by Hyderabad (81.066), Nawabshah (81.066), Mirpurkhas (70.333) and Sanghar (58.333) The

morbidity rate, mortality rate and case fatality rate averaged 32.55%. 14.18% and 22.94%

respectively

214

CONCLUSIONS AND RECOMMENDATIONS

Coccidiosis showed a rising trend of occurrence with the increasing flock sizes. Besides

due to comparatively higher prevalence or morbidity rates, this disease is considered to be

a disease of high priority from control point of view (Table 10). Since this disease prevails

due to faulty management, it is therefore recommended that strict hygienic measures on

the farms be adopted to control the occurrences of outbreaks of Coccidiosis. Burn or

remove litter or other refuse which may be contaminated with infected droppings

Ammonia fumigation has been used successfully in destroying oocysts in poultry houses

Brooders and litter should be kept as dry as possible through correcting the ventilation.

Selection of poultry strains for genetic resistance to Coccidiosis be given importance

Many varieties of anticoccidials are available in the market for prevention of Coccidiosis

but continuous use of those drugs should be avoided.

The morbidity per farm of Marek's disease was 25..> percent and the occurrence of this

disease also showed a rising trend in all the districts with increasing population of the birds

on the farms This disease is given second priority after Coccidiosis (Table 10). To control

outbreaks of Marek's disease vaccination should be performed at one day of age. w hich

prevent the birds throughout life The virus of Marek's disease spreads veiy slowly in

chickens resistant to this disease; therefore emphasis be given to the propagation of

genetically resistant stock for prevention of this disease.

Newcastle disease ranked as third important disease (Table 10) of the commercial broiler

and layer poultry farms of Sindh with morbidity rate per farm of 24.75 percent The

disease showed a rising trend. Newcastle disease has a high morbidity and high mortality-

rate To control the disease, systematic regular and timely vaccination schedule be

adopted Ensure the prevention of contact of the vims with susceptible birds. Birds

contact natural infection, if placed in infected premises and the ground remains infective

for 7 weeks after removal of sick birds. Sanitary management and correct disposal of

215

»>

hatchery wastes, manure and dead birds by burial or burning must strictly be followed All

unauthorized entries, even of human beings, into the battery brooders be stopped

Chronic respiratory disease ranked as fourth important disease (Table 10) with morbidity

per farm 23.99 percent. This disease also showed a rising trend. To control the outbreaks

of CRD chicks, growers may be kept away from the adult Hock. Vaccination for the

breeders and layers is also recommended to control this disease. For treatment antibiotics

have been found to exert inhibitory effects.

Fowl pox was reported from majority of broiler and layer commercial poultry farms

throughout the Sindh province and ranked as fifth important disease (Table 10) with

morbidity per farm 21.06 percent with a slightly increasing trend. Fowl pox vaccine

prepared from selected strains of the virus confers immunity lasting for about one year

The best age for vaccinating birds is six to eight weeks. Vaccination should not be delayed

till laying starts, since it almost invariably results in a drop in a production.

Infectious coryza ranked as sixth important disease (Table 10) with morbidity per farm

20.67 percent. The disease showed a rising trend. To prevent and control the disease, it is

advised that birds recovered from this disease are reservoirs of infection hence should be

removed from the flock and premises should be dis-infected before bringing in new batch

of chicks. Sanitation and proper ventilation will aid in prevention.

Lymphoid leukosis ranked as seventh important disease (Table 10) with morbidity per

farm 20.36 percent and showed a rising trend. For the control of the disease, it is

recommended that virus should be eradicated by the breeding farmers.

Fowl cholera ranked as eighth important disease (Table 10). Sanitation has very important

role in the control of this disease. Carcasses may be disposed of very' quickly from the

farms. A combination of vaccination, strict hygiene and an effective antibiotic cover can

help to greater extent in prevention of the disease. Vaccination containing several

serotypes of bacterium be used.

Gumboro disease ranked as ninth important disease (Table 10) with morbidity per farm

19.74 percent. The disease showed a rising trend in all the districts under study except in

216

j

Karachi where the disease showed a secular trend. It is recommended that strict hygienic

measures be adopted, bedding should be destroyed and poultry houses may be well

cleaned to control the disease. Use of vaccine prevents the disease and gives satisfactory

protection when given at 1-7 days of age.

Salmonellosis ranked as tenth important disease (Table 10) and showed comparatively

higher morbidity rates than the mortality rates. The rising trend of this disease obtained in

the present study warrants more drastic disease control measures at hatchery as well as at

poultry farm level. Birds of different ages should not be mixed, cleanliness of the premises

where the young chicks are reared should also be performed to avoid outbreaks. It is

important to provide standard commercial feed because poultry feeds are sometimes

contaminated w ith serotypes of the Salmonella group and to control the Salmonellosis it is

recommended that bacteriological examination of fish meal, meat meal and bone meal sold

in market be carried regularly.

Colisepticaemia ranked as eleventh important disease (Table 10) with morbidity per farm

I I 85 percent. The disease showed a rising trend and warrants effective sanitation

programme.

Angara disease (Hydropericardium Syndrome) was mainly reported in broilers and rarely

in layers with morbidity per farm 11.54 percent. Angara disease ranked as twelfth

important disease (Table 10) To control the outbreaks of this disease, it is recommended

that poultry sheds should be kept vacant for atleast two weeks before using again, during

the rest period spray with antiviral and antibacterial disinfectants should be adopted atleast

five times, dead birds should be immediately removed and burned. Angara vaccine should

be given at 10-14 days of age.

Fowl typhoid ranked as thirteenth important poultry disease (Table 10) with morbidity per

farm 9.7 percent. The disease showed a secular trend. For effective control of this disease

isolation and identification of the causal organism should be performed in the laboratory'.

the whole group of chicken in which the disease is present should be tested with the

w'hole blood method, using the stained Salmonella pullorum antigen.The reactor birds

should be disposed of and the non-reactors should then be separated.

217

Appendix - 1:

Monthwise number of outbreaks of various diseases on commercial poultry farms of Sindh for the year 1978.

Number of Outbreaks

DiseaseTotalAug Sept Oct Nov DecJan Feb Mar Apr May Jim Jul

151. Salmonellosis 02 7 70 04

102. CRD 0 *> 00 00

3 Colisepticaemia

4. Fowl Cholera

5. Infectious Coryza

6. Fowl Typhoid

7. Fowl Pox

8. Gumboro Disease

9. Lymphoid Leukosis

10. Marek's Disease

1 1 Newcastle Disease

12. Hydropericardium

13 Coccidiosis

20 0 0 0 0 0 0 00 0

00 0 0 0 00 0 0 0 00 0

00 0 0 00 0 0 0 0 0 00roh-*

CD00 0 0 40 7 0 0 0 0 0 7

00 0 0 0 0 00 0 J

00 0 0 0 0 10 0 0 0 0

70 0 00 0 0 0 0 0 7*1A

0 0 310 4 17 0 04/>

197 04 4 0 07 ->

0 00 0 00 0 0 0 0 0 00

5 4944 4 7 4>.5 J -»

Total : 8 10 9 16 24 14112 8 S1 9 106

/

•\

"“I

,\ppeiiui\ - i. :

Monthwise number of outbreaks ol' various diseases on commercial poultry farms of Sindh for the year 1979.

Number of Outbreaks

DiseaseJail Feb Mar Apr May Jun Jul Aug Sept Oct Nov Dec Total

1 . Salmonellosis 030 0 0 490 0 0l.1

2. CRD 50 0 l 0 0 15J

3. Colisepticaemia

4 Fowl Cholera

5. Infectious Coryza

6. Fowl Typhoid

7. Fowl Pox

8 Gumboro Disease

9 Lymphoid Leukosis

10. Marek’s Disease

I I Newcastle Disease

0 00 0 00 0 0 0 00 0 0

00 00 0 00 0 0 0 4fO

0 0 0 0 0 0 0 0 0 0 0I—’ J

0 1 06 1 0 0l ~> 0 0 J

0 0 00 0 1 0 0 6

00 0 02 0 0 0 0 0 0 ~>0

52 0 2 0 04 ->J

0 0 0 150 0J.1 J

9 06 4 ~> ~> ~> 406

012. Hydropericardium

13 Coccidiosis

0 0 00 0 0 0 0 0 0 0 0

420 1 710 4 76.1 .1 j

Total 15 52 52 14 7 12 I! IS 5 24517 9

t

.x.

Monthwise number of outbreaks of various diseases on commercial poultry farms of Sindh for the year 1980.

Number of Outbreaks\

Disease TotalAug Sep t Oct Nov DecJan Mar Apr May Juu JulFeb

1. Salmonellosis 70 0 0 00 0 20

2. CRD 0 0 01 0 0 0 0 1 50 0

3. Colisepticaemia

4. Fowl Cholera

5. Infectious Coryza

6. Fowl Typhoid

7 Fowl Pox

8. Gumboro Disease

9. Lymphoid Leukosis

10 Marek's Disease

l ! Newcastle Disease

0 0 0 0 0 0 10 0 00 0

0 0 0 00 0 0 0 0 00 0 0

0 0 00 0 0 0 0 00 0NJ

o 0 00 0 0 0 0 00 0 0 00

1 0 0 0 I 0 0 40 0 0

00 0 0 0 00 0 0 00

10 04 0 214 0 .1.1.1

0 0 "ÿ> 0 I 214Is .1 .)

4 244 -> 0 4

12. Hydropericardium

13 Coccidiosis

0 00 0 0 0 0 0 00 0 0 0

•}I -> 261 i"ÿ>6

Total 14 4 14 10 8 76

/

Monlliwise number of outbreaks of various diseases on commercial poultry farms of Sindh for the year 1981.1

Number of Outbreaks

DiseaseTotalJan Feb Mar Apr May Jun Jill Aug Sept Oct Nov Dec

1 Salmonellosis 230 9 00 2 0 0 I2 .>J

2. CRD 15-> ~> 00 I 0 0 0 4

3 Colisepticaemia

A Fowl Cholera

5. Infectious Coryza

6. Fowl Typhoid

7 Fowl Pox

8 Gumboro Disease

9. Lymphoid Leukosis

10. Marek's Disease

1 1 Newcastle Disease

00 0 00 0 0 0 00 0 0 0

0 00 0 0 0 0 0 00 0 0 0

2 0 120 n 0 0JV)

00 0 0 0 0 00 0 0 0 0 0

0 0 0 0 6-> 0 0 0

0 00 0 0 0 00 0 0 0 0 0

200 02 0 1 s0 4 4

0 0 23~> 5i 7 003 -ÿ>

8 10 0 878 7 191 I 7 .1

12. Hvdropericardium

13. Coccidiosis

000 0 0 0 0 0 0 00 0 0

5 4 8 7 656 5 16 >-I

Total : 16 20 22 23 ~n 25128 24 24 43 810

f

.V

1

Appendixo :

Montlrwisc number of outbreaks of various diseases on commercial poultry farms of Sindh for the year 1982.

Number of Outbreaks

DiseaseTotalJan Feb Mar Apr May Jim Jul Aug Sept Oct Nov Dec

251 Salmonellosis 2 ~>I 4 45

2 CRD 7 327 5~> 0 0 00 4 .1

3. Colisepticaemia

4 Fowl Cholera

5. Infectious Coryza

6. Fowl Typhoid

7. Fowl Pox

8 Gumboro Disease

9. Lymphoid Leukosis

10. Marek’s Disease

1 1. Newcastle Disease

0 00 0 0 0 00 0 0 0 0 0

00 0 0 0 0 00 0 0 0 0 0

320 4 -> 44 4 J

00 0 0 00 0 0 0 0 0 0 0

000 0 0 0 0 0 00 0 0 0

00 00 0 0 00 0 0 0 0 0

0 0 0 100 00

00 0 0 70 0 0 0 0 0

8 7 43I 6 40 6

12. Hydropericardium

13. Coccidiosis

0 0 0 0 00 0 0 0 0 0 0 0

1 539 7 4 5 5 6

Total : 15 7 19 IS 20 19 17 196 21 ~n 19815

t

Montliwise number of outbreaks of various diseases on eoiumerciai poultry farms of Sindh for the year 1983.

Number of Outbreaks

DiseaseTotalJan Feb Mar Apr May Jim Jui Aug Sept Oct Nov Dec

I. Salmonellosis 0 2 14I 4 -> 0 0

2. CRD 90 0 0 0 00 n

3. Colisepticaemia

4. Fowl Cholera

5. Infectious Coryza

6. Fowl Typhoid

7 Fowl Pox

8. Gumboro Disease

9, Lymphoid Leukosis

10. Marek's Disease

1 1. Newcastle Disease

0 0 0 0 0 0 0 0 0 I 0 0

0 0 0 0 0 0 0 0 00 0 0 0

0 0 0 0 0 0 00 0 0 0 0 0

00 0 0 0 0 0 20 0 0 0

0 50 0 0 0 I 0 0 0

0 0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 70 -> 0 1.1

0 0 170 4 314 0 0

4 2 04 ~> 19I 0 0

12. Hydropericardium

13. Coccidiosis

0 0 0 0 0 0 0 0 0 0 0 0 0

m

4 4 *> 494 4.'i

Total : 98 9 1 (> 24 12 8 6 21 9 7 1389

/

<v

Monthwise number of outbreaks of various diseases on commercial poultry farms of Sindh for the year 1984.

Number of Outbreaks

DiseaseJan Feb Mar Apr May Jim Jul Aug Sept Oct Nov Dec Total

I Salmonellosis 0 0 I I 00 0 I 0 0 6

2 CRD 00 0 0 0 0 00 0

-v Colisepticaemia

4 Fowl Cholera

5. Infectious Coryza

6. Fowl Typhoid

7. Fowl Pox

0 0 0 0 00 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 00 0

0 0 0 0 0 0 0 0 00 0o

0 0 00 0 0 00 0 0 0

0 0 0 0 0 I 0 0 0 0 0 I 1

8. Gumboro Disease 0 0 0 0I 0 0 0 0 0 0 0 I

9. Lymphoid Leukosis

10. Marek's Disease

I 1 Newcastle Disease

0 4 0 210 04

0 04 210 ->4

44 0 24->4

12. Hydropericardium

LV Coccidiosis

00 0 0 0 0 0 0 0 00 0 0

4 27I 6

Total : 14 5 10 8 1 1070 6.5 .1 a

/

Appcndix-8 :

Monthwise mimbcr ol' outbreaks of various diseases on commercial poultry farms of Siudli for (lie year 1985.

Number of Outbreaks

DiseaseTotalAug Sept Oct Nov Dec-Jail Feb Mar Apr May Jun Jul

I. Salmonellosis 12 4204 8 8I .>

2 CRD 9 9 522 90 I 4 0 4 6r'.1

3. Colisepticaemia

4. Fowl Cholera

5. Infectious Coryza

6. Fowl Typhoid

7. Fowl Pox

8. Gumboro Disease

9 Lymphoid Leukosis

10 Marek's Disease

I I Newcastle Disease

00 0 0 00 0 0 0 0 000

00 0 0 0 0 00 0 0 0 00

10 48I 0 ~> 84 64 63

0 0 0 0 00 0 0 0 00 0 0

0 0 0 00 0 0 00 0 0

0 0 00 0 00 0 0 0 0 00

00 540 00 13 1 14 0

00 0 0 84 0 00

9 0 12 15 4 9027 9 8

12. Flydropericardium

1 3. Coccidiosis

0 0 00 0 0 0 0 00 0 00

19-) 0 7 20 15 4 16 I 1516.3 .3

Total : 17 8 216 19 68 43 42 63 6357 410

t

A.

r!J

Monthwise number of outbreaks of various diseases on commercial poultry farms of Sindh for the year 1986.

Number of Outbreaks

DiseaseJan Feb Mar Apr May .Jun .)nl Aug Sept Oct Nov Dec Total

17 I JJI. Salmonellosis 17 1210 17 7 10 12 12 144

902 CRD 0 10 15 6 90 4 S 6 16

3. Colisepticaemia

4. Fowl Cholera

5. Infectious Coryza

6. Fowl Typhoid

7. Fowl Pox

100 0 010 0 0 0 0 0 0 0 0

0 0 00 0 0 0 0 0 0 0 0 0

7 7 566 i 2 I I 7 44 jj

0 00 0 0 0 0 0 0 0 0 0 0

0 0 0 0 40 0 0 0 1 0

8. Gumboro Disease

9. Lymphoid Leukosis

10. Marek's Disease

00 0 0 0 I 0 0 0 0 0 0

*1 5 5 626 4 10 12 6 .ÿ>.>

270 s 9 5 0 00 0 0I

1 1. Newcastle Disease 23 27 157 8 10 17 17 16212 9 6

12. Hydropericardium

1 3. Coccidiosis

0 0 0 0 0 0 0 00 0 0 0 0

1 25 24815 32 28 30 23 20 27 13 15.>

Total : 34 56 63 73 77 99 73 68 63 5;, 59 80082

•ÿsaw*

Appendix - 11) :

Mouthwise number of outbreaks of various diseases on commercial poultry farms of Sindli for the year 1987.

Number of Outbreaks

DiseaseTotalJan Feb Mar Apr May Jim Jul Aug Sept Oct Nov Dec

I . Salmonellosis 21 16624 20 IS S 14 15 15 15 76

2 CRD 9312 8 9 4 0 8 8 6 410 16 S

3. Colisepticaemia

4. Fowl Cholera

5. Infectious Coryza

6. Fowl Typhoid

7. Fowl Pox

8. Gumboro Disease

9 Lymphoid Leukosis

10. Marek's Disease

1 1 Newcastle Disease

12518 13 25 13 96 9 1 1 7 0 86

0 20 0 0 0 0 0 0 00

0 0 6 j 0 10 5 484 7 6)

0 0 0 0 0 0 00 0 0 0 0 0]

0 0 0 0 0 0 40 0 I

0 0 0 0 0 0 00 0 0 0 00

4 514 49 4 4 6J

0 0 0 0 90 0 0 00a

12 12 13 1209 10 s I1 1 6

12. Hydropericardium

13. Coccidiosis

0 0 0 0 0o 0 000 00 0

157 -> 72S7 46

Total : 68 74 80 60 54 32 50 60 69065 57 49 44

vt f

Appendix-ii :

Montlixvise ntunber of outbreaks of various diseases on commercial poultry farms of Simlh for the year 1988

Number of Outbreaks

DiseaseJan Feb Mar Apr May Jun Jul Aug Sept Oct Nov Dec Total

I . Salmonellosis 15 23 19 19523 9 8 15 1312 12.l.i J

2 CRD 54 12 980 266 0 99.1 .i

3. Colisepticaemia

4 Fowl Cholera

5. Infectious Coryza

6 Fowl Typhoid

7. Fowl Pox

8. Gumboro Disease

9. Lymphoid Leukosis

1 0 Marek's Disease

I 1 . Newcastle Disease

910 17 7412 12 6 -> 0 0I .ÿ>

0 0 0 0 0 0 00 0 0 0

7 6 4 9 644 4 8 .i

0 0 00 0 0 00 0 0 00 0

0 0 0 0 0 00 0 00 0

00 0 0 0 0 0 0 0 0

~> 05 0 70 290 4.i .1

0 0 0 4 0 0 120 00.1

15 i 13 70 7 9 8484.1

12 Flydropericardium

13. Coccidiosis

0 00 0 0 ! 236 8 s

157 8 12 15 5 S 8 10 1 1614

Total : 50 86 92 62 60 37 51 41 47 47 7453 700

/

.SS. •

Appendix- 12 :

Montliwise number of outbreaks of various diseases on conuuercia) poultry farms of Sindh for the year 1989.

Number of Outbreaks

DiseaseTotalAug Sept Oct Nov DecJan Mar Apr May Jun JulFeb

l. Salmonellosis 17 13212IS 22 12 ~> 1 96.ÿ>

2. CRD 17 8910 79 8 7 7 S >

3. Colisepticaemia

4. Fowl Cholera

5. Infectious Coryza

6. Fowl Typhoid

7. Fowl Pox

S. Gumboro Disease

9. Lymphoid Leukosis

10. Marek's Disease

1 1 . Newcastle Disease

767 10 12 0 06 12 9 4 8 5

01 0 0 0 00 0 0 0 0 00

649 02 9 10 26 84 I

0 0 0 00 00 0 0

0 70 0 0 0 0 0 0

0 0 00 0 00 0 0 00

4 46 9113 9 16 916 3 .i

0 S0 0 140 0 00 0 .1

9416 10 6 4 10 10 46

12. Hydropericai'dium

13 Coccidiosis

~> 0 0 268 0 0 s 0I.s

17 12 7 1 196 910 10 8 4

Total 78 86 80 64 40 66 71842 60 34 3956.v>

%f

•v -*-

1Appendix-13 :

MontInvise number of outbreaks of various diseases on commercial poultry farms of Sindh for the year 1990.

Number of Outbreaks

DiseaseTotalAug Sept Oct Nov DecJail Fch Mar Apr May Jun Jul

19!91013 19! . Salmonellosis 24 15 8 477 19 35 .i

4477 72 CRD 0 77 10 4 6>

643. Colisepticaemia

4. Fowl Cliolera

5. Infectious Coryza

6 Fowl Typhoid

7 Fowl Pox

8. Gumboro Disease

9. Lymphoid Leukosis

10. Marek's Disease

1 1 . Newcastle Disease

-> 012 7 713 710 I I

4000 07 0 0 00 0

5697 97 7 40 76 .1

94 07 0 00 0 00M

o6005 0 0 00 0 00 0

80 00 0 07 0 07 7

8 447 5 97 00 67.1

42070 7 8 00 0 1 1 9J

6810 95 8 412 9

3812. Hvdropericardium

13 Coccidiosis

076 4-7 77.1

97766 4 10I I I I 104 16 6

67147 34Total : 78 75 65 68 50 4732 48 SO 68

f

Appendix-14 :

Monthwise number of outbreaks of various diseases on commercial poultry farms of Sindh for the year 1991.

Number of Outbreaks

DiseaseTotalAug Sept Oct Nov DecJail Feb Mar Apr May Jun Jul

2231. Salmonellosis 17 15 20 1716 23 17 23 12 2-120 10

302. CRD 11 i 1 71 6> .i

533. Colisepticaemia

4. Fowl Cholera

5. Infectious Coryza

6. Fowl Typhoid

7. Fowl Pox

S. Gumboro Disease

0. Lymphoid Leukosis

10. Marek's Disease

1 1 Newcastle Disease

7 87 9 4.1

i

0 0 4 40 0 46 7

449i 77 4 7 4 7.ÿ>

N)

0 90 00 7 7 0U)

I—1

0 0 400 0 0 00

6277 8 7 7 S0 7 97

417 7 1 4447 7 777 7

250 0 9 80 0.i

1 10029 128 106 6 07 77

12. Hydropericardium

13. Coccidiosis

797 6 1076 S 6.-'l ;>

547 7 7 74 7 44 44 6 7

Total 82752 54 55 74 8645 45 91 77 6793 88

/

—

Appendix-15 :

Montliwise number of outlireÿiks of various diseases on commercial poultry farms ol Simlli for t lit* year 1992.

Number of Outbreaks

DiseaseTotalAu« Sept Oct Nov DecMar Apr May Jim JulJan Feb

1081 . Salmonellosis 19 24 1310s

9 9 60 .ÿ>.>

2. CRD 4976 7 4-> 4 9->.>

-v Colisepricaemia

4 Fowl Cholera

5 Infectious Coryza

6. Fowl Typhoid

7. Fowl Pox

73~>10 n o 9 94 . 6 ~>

3504 90 -> 4 44 4

39 .7 60 0 06 0 4s

0 00 0 0 0 0 0 00 0 0 0N3

u>M

0 0 0 0 I0 0 0 0 0 J

678 Gumboro Disease

9. Lymphoid Leukosis

10. Marek's Disease

3 S9 7 7 II 0 0

420 0 7 90 -> 4.ÿ>

280 04 ~>S ->4

I I . Newcastle Disease

1 2. Hydropericardium

13. Coccidiosis

10 9 1 101515 10 10 1414 8 .1

5777 5 5 .5 10 08 0 4 .1 y

5770 13 104 5J

66827 36 64 100 63 71Total : 82 60 51 61 47 6

t

CHAPTER - VI

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