Leg problems due to nutritional and bacterial diseases in ...vetmedbas.com/wp-content/uploads/2017/02/قييصر-1.pdf · Basrah university in partial fulfillment for ... staphylococcosis

Leg problems due to nutritional and bacterial diseases in chickens

A thesis

Submitted to the college of veterinary medicine of Basrah university in partial fulfillment for the degree of

high diploma of science in veterinary medicine / pathology and poultry disease

By

Kayser Lazam Shanoob

B.V.M.S. 2008

Supervisor

Professor

Ali A.S. AL-Mayh

2010 A.D 1431A.H

حیـــم ن ٱلر حم ٱلر حیـــمبســــم ٱ ن ٱلر حم ٱلر بســــم ٱ

ذین ءامنوا منكم رفعرفع﴿ی ﴿ی ٱل ذین ءامنوا منكمٱ ٱل ◌ ◌ ٱ◌ین ◌ین وٱلذ ◌ أأوٱلذ ◌ وتوا ٱلعلم درجات وٱ وتوا ٱلعلم درجات وٱ

ون خبیر﴾ ون خبیر﴾بما تعمل بما تعمل

ٱلعلي ٱلعظیم ٱلعلي ٱلعظیم صدق ٱ صدق ٱ

)١١آیة (سورةالمجادلة

ACKNOWLEDGEMENT

It's from absolute oneness of God from no God but Allah alone. I thank

God for His support and influence in my life and work. Not only did He

provided the project of my interest, He encouraged me through the

assistance of the expertise of many knowledgeable and caring people.

I thank for my supervisor professor Dr. Ali A. S. Al-mayah for his

supervision and his providing for me with the opportunity to achieve

this thesis .

Iam grateful for Dean of Veterinary Medicine College assistant

professor Dr. Basil A. Abbas. I would like to thank Dr. Adnan AL-Rodhan

the Head of Department of Pathology and Poultry Diseases

Also lecturer Qaissar Ali, Hasan kareem , Nbeel Mahdi, Hekmat Kadhim

,muslim Dhaher, Sadiq Iubaies , Mohammed Aumran , Iosama Ismaiel ,

Haider Flaeh ,Salah Mahdi ,Dr. Dhurgham Ali ,Haedar flaih

kayser

2010

Certification

I certify that this thesis was prepared under our supervision at the

Department of Pathologyand Poultry Disease / College of Veterinary

Medicine / University of Basrah, as a partial requirement for the higher

diploma Science degree in Veterinary Medicine (poultry Disease).

Signature

professor

Ali A.S. ALMayah

The recommendation of the Head of the Department

In view of the available recommendation, I forward this thesis for

debate by the examining committee.

Signature

Assistant professor

Dr. Adnan Al-Rodhan

Head of Department of Pathology

and poultry disease

College of Veterinary Medicine

University of Basrah, Iraq.

Certification of Examining Committee

We, the members of examining committee, certify after reading

this thesis ((Leg problems due to nutritional and bacterial diseases in

chickens)) and after examining the student in it's content, we found it

is adequate for the award the higher diploma Science degree in

Veterinary Medicine in Microbiology. With excellent degree.

Signature

professor

Dr.Fawziah A.Abdulla

Chairman

Signature Signature

professor Lecturer

Ali A.S.Al-Mayah Dr.Mohammed A.Y.Al-Amery Member and Supervisor Member

Approval for the College Committee on graduate, studies.

Signature

Assistant professor

Dr. Basil A. Abbas

Dean

College of Veterinary Medicine

University of Basrah, Iraq.

Date of examina on: 23 – 11– 2010.

List of Abbreviations

IUPAC International Union of Pure Applied Chemists

1α,25(oH)2D3 1α,25hydroxycholecalciferol

TPP Thamine PyroPhosphate

NAD Nicotenamid Adenine Dinucleotid

NADP

APEC

Nicotenamid Adenine Dinucleotid Phosphate

Avian Pathogenic Escherichia coli

ELISA

Enzyme-Linked Immunosorbent Assays

Summary

In this study chickens legs problem were determined and divided according to their causes into tow major groups .

1-Nutritional causes.

2-Bacterial causes.

In this study revealed that the legs problem due to nutritional diseases

causes the problem was due to low concentration of vitamins in ration and the example.

Vitamin D deficiency , vitamin B1deficiency ,vitamin B2 deficiency, vitamin E deficiency and vitamin A deficiency.

For bacterial diseases were acompiand with pathologyical lesion in the legs some of the most important diseases show leg problem as follow

Colibacillosis. Mycoplasma synoviae infection, pullorum disease, fowl typhoid ,staphylococcosis and Botulism.

CHAPTER 1

INTRODUCTION

Introduction

Diseases of poultry legs which caused by mal nutrition and bacterial

diseases is one of important for veterinarian as well as its importance with

owners ,farmers to give the practical and scientific information above

poultry diseases for benefit in poultry management (Al zubaidi,1986).

for this mentioned so,this study included the fallowing diseases were in

due to leg problems

Nutritional diseases included : Vitamin D deficiency , vitamin

B1deficiency (Thiamine),vitamin B2 deficiency(Riboflavin),vitamin E

deficiency (Encephalomalacia) , vitamin A deficiency (Mankin, 1994)

and bacterial diseases which included Colibacillosis , Mycoplasm

synoviae infection , staphylococcosis , pullorum disease , fowl typhoid ,

Botulism (Davies, 2004).

The aims of study

This study aimed to know the important diseases of malnutrition and

bacterial infection which cause the problems of chickens legs ; where the

knowing of pathogenesis, clinical signs, diagnosis and methods of

treatment. As well as, benefit for veterinarians

Aims of the study This study aimed to know and study the important diseases of

malnutrition and bacterial infection which cause the problems of chickens

legs; where the knowing of pathogenesis, clinical signs, diagnosis and

methods of treatment. As well as, to benefit for both veterinarians and

students.

CHAPTER 2

REVIEW OF LITERATURE

2- Review of literatures:

2.1-Nutritional diseases

2.1.1- Vitamin A deficiency

Vitamin A is essential in poultry diets for growth, optimal vision, and

integrity of mucous membranes. Because epithelial linings of alimentary,

urinary, genital, and respiratory systems are composed of mucous

membranes, these tissues in which lesions of vitamin A deficiency

are most readily observed (Whitehead,1998).

Signs

Vitamin A deficiency signs in chicks and poults are characterized by

cessation of growth, drowsiness, weakness, incoordination, emaciation,

and ruffled plumage. If deficiency is severe, they may show ataxia

(Whitehead,1998).

Postmortem lesion

Histopathology of vitamin A deficiency in young chicks revealed

marked retardation and suppression of endochondral bone growth. The

proliferating zone is reduced. Hypertrophied cells

accumulate,surrounded by uncalcified matrix. Vascular invasion of the

epiphyseal cartilage is reduced and exhibits irregular patterns such as

branching. The number of endosteal and periosteal osteoblasts is

decreased, leading to impaired bone growth and thinning of bone cortex

(Wong,1999).

Diagnosis

Vitamin A deficiency can be diagnostic by clinical signs ,post mortem

lesion and its level evaluation in diet (Wong,1999).

Differential diagnosis

Vitamin A deficiency differentiated from vitamin E deficiency by

histologic examination of the brain; Periorbital edema may occur.Clinical

signs and lesions of vitamin A deficiency of the respiratory tract are

variable; it is difficult to differentiate this condition from infectious

coryza, fowl pox, and infec ous bronchi s (Wong,1999).

Treatment

Poultry found to be severely deficient in vitamin A should be given a

stabilized vitamin A prepara on at a level of approximately 10,000 IU

vitamin A/kg of ration. Absorption of vitamin A is rapid؛ therefore,

chickens not in advanced stages of deficiency should respond promptly,

except for blindness، which may be permanent (Whitehead,1998).

Vitamin D

Structure of vitamin D

Bartholomew et al.,(1998) refers to a family of vitamin D compounds

that possess antirachitic activity. Members of the family are derived from

the cyclo-pentanoper hydro-phenanthrene ring system which is common

to other steroids, such as cholesterol . However vitamin D has only three

intact rings ; the B ring has undergone fission of the 9,10 carbon bond,

resulting in the conjugated triene system of double bonds that is

possessed by all D vitamins. The structure of vitamin D3 is shown in

Fig(1).

Fig(1).The structure of vitamin D3 and D2 (Bartholomew et al., 1998).

This figure show the chemistry and irradiation pathway for production of

vitamin D3 (a natural process) and vitamin D2 (a commercial process).

In each instance the provitamin, with a Δ5,Δ7 conjugated doublebond

system in the B ring, is converted to the seco-B previtamin, with the 9,10

carbon–carbon bond broken (Bartholomew.,et al1998).Then the

previtamin D thermally isomerizes to the ‘‘vitamin’’ form, which

contains a system of three conjugated double bonds. In solution vitamin

D is capable of assuming a large number of conformations due to rotation

about the 6,7 carbon–carbon bond of the B ring. The 6-s-cis conformer

(the steroid-like shape) and the 6-s-trans conformer (the extended shape)

are presented for both vitamin D2 and vitamin D3(Edwards, 1994).

Vitamin D synthesis

Vitamin D designates a group of closely related compounds that

possess activity against vitamin deficicency.The two most prominent

members of this group are ergocalciferol (vitamin D2) and

cholecalciferol (vitamin D3)fig(1). Ergocalciferol is derived from a

common plant steroid, ergosterol and is the form that was employed for

vitamin D fortification of foods from the 1940s to the 1960s.

Cholecalciferol is the form of vitamin D obtained when radiant energy

from the sun strikes the skin and converts the precursor 7-

dehydrocholesterol into vitamin D3. Since the body is capable of

producing cholecalciferol, vitamin D does not meet the classical

definition of a vitamin (Ameenuddin etal., 1985).

Physiology of Vitamin D

The principle physiology function of vitamin D is to facilitate

absorp on of calcium of the diet within the intes ne, which is 1,25(OH)

2D acts by s mula ng the expression of a number of different proteins

that assist with calcium transport from the intestine into the blood

stream (Rennie et al.,1993) .

If the body does not have enough calcium in the blood stream it

attempts to increase circulating calcium levels by releasing parathyroid

hormone. Parathyroid hormone has three function that compensation

for insufficient intestinally derived calcium: mobilization of calcium from

bone, inducing the produc on of 1,25(OH)2D in the kidney and the

suppression of calcium wasting in urine . When circulating calcium levels

are below normal the body extracts calcium from stores in order to

sustain nerve and muscle function meaning that having a healthy level of

vitamin D is related to works in concert with a number of other vitamin

minerals , and hormone to promote bone mineralization (Rennie et

al.,1993) .

2.1.2-Vitamin D deficiency

Vitamin D is required by poultry for proper metabolism of calcium and

phosphorus in the formation of normal skeletal bones, hard beaks and

claws, and strong eggshells. It functions in the regulation of calcium

metabolism by stimulating the intestinal absorption of calcium,

influencing osteoblast and osteoclast activity and increasing renal

tubular reabsorption of calcium in response to metabolic demands for

calcium (Edwards,1994).

Pathogensis of vitamin D deficiency

In chronic vitamin D deficiency marked skeletal distortions become

apparent poor calcification can be observed at the epiphysis of the tibia

or femur. Bones of vitamin D deficient chicks have reduced calcium

content with an increased proportion of osteoid and a greater

proportion of bone mineral is present as a low density amorphous form

of calcium phosphate (Heinz and Hoffman, 1996) .

The ratio of dihydroxylysinonorleucine to hydroxylysinonorleucine in

bone collagen is increased Vitamin D deficiency results in widening of

the epiphyseal plate, hypertrophy, and softening of bone.As the

deficiency progresses, the columns of chondrocytes in the degenerating

hypertrophic zone of the epiphyseal plate become shortened and

thickened and exhibit an irregular pattern of invasion by metaphyseal

blood vessels. Irregular patterns of cartilage and bone development

occur in the primary and secondary spongiosa .Porosity of cortical bone,

sometimes leading to fractures , increases due to resorption of bone in

haversion canals, fractures also may occur elsewhere decrease in

trabecular bone volume due to increased osteoclast resorbing activity

contributes to diminished mechanical strength of long bones (Heinz and

Hoffman, 1996) .

Increasing the dietary calcium level to levels twice those normally

required maintains normal epiphyseal cartilage width and metaphyseal

bone histomorphology and mineralization inchicks fed vitamin D

deficient diets . (Fuhrmann and Sallmann,2000).

Types of vitamin D deficiency

2.1.2.A. Ricket

2.1.2.B. Osteomalacia

2.1.2.A. Ricket

Rickets a disease of vitamin D deficiency occur in chickes is defined as

a generalised osteodystrophy in which poor mineralisation is the main

pathological feature. The occurrence of rickets is in the great majority

of cases, due to an error on the part of the food compounder, usually in

omi ng vitamin D3 from the premix or in failing to supply an adequate

level of available phosphorus. Rarely rickets may result from a

metabolic defect in the liver or kidney which prevents vitamin D3 from

being converted to its physiologically active form (Balnave, 2004) .

Clinical signs

show the first sign of vitamin D deficiency in chicks is rickets (rubbery

leg) characterized by severe fragility and bending of long bones due to

poor mineralization, birds walk with obvious effort and take a few

unsteady steps before squatting on their hocks,they rest swaying slightly

from side to side(Rennie etal.,1993; Kannan etal.,1997)

Postmortem lesion

Baksh,(1994) has refer to enlarged of end bonein rickets.Poor

calcification can be observed at the epiphysis of the tibia or femur.

Bones of vitamin D deficient chicks have reduced calcium content with

an increased proportion of osteoid and a greater proportion of bone

mineral is present as a low-density amorphous form of calcium

phosphate(Seo et al.,1997).

Histopathology

Histopathological changes in bones include widening and

disorganization of the zones of hypertrophy of the growth plates which

are poorly penetrated by metaphyseal blood vessels and thus poorly

calcified, there also tends to be replacement of bone marrow by fibrous

tissue in advanced cases of ricket (Daghir,2009).

2.1.2.B. Osteomalacia

Osteomalacia is defective mineralization of bone matrix (osteoid) and

results from vitamin D deficiency in adult chickens ( Warrell et al.,2003).

Vitamin D is required for effective calcium absorption, it is absorbed

from the gut as ergocalciferol (vitamin D2) and (cholecalciferol; vitamin

D3) or made from 7-dehydrocholesterol in the skin as cholecalciferol.

Both vitamin D2 and vitamin D3, collectively known as vitamin D are

stored in fat. Circulating vitamin D is then hydroxylated in the liver to 25-

hydroxyvitamin D and again in the kidney (under feedback control) to

1,25-dihydroxyvitamin D the ac ve form (Eyles, 2003).

Clinical Signs

In confined laying hens signs of deficiency begin to occur as soon as 2

weeks after they are deprived of vitamin D. Individual hens may show

temporary loss of the leg use ,during periods of extreme leg weakness

hen show a characteristic posture that has been described as a penguin-

type squat ( Seo et al.,1997; Ban, 2000).

Postmortem

In laying and breeding chicken receiving deficient vitamin D

characteristic changes observed on necropsy are confined to bones.

Bones are soft and break easily , widening of the epiphyseal and

softening of bone. Enlargement of the epiphyseal plate initially is due to

widening of the proliferating and hypertrophic zones as the deficiency

progresses. Another skeletal disorder tibial dyschondroplasia

frequently is observed in broiler chickens (Breves and Schröder, 1991)

Diagnosis of Vitamin D deficiency

A-Signs:

The first sign of rickets tends to b ataxia without necessarily a

depressed rate of growth or any gross skeletal deformity. The sense of

touch is of more use than that of sight in making a rapid tentative

diagnosis. Skeletal deformities develop much later and those most

prominent are dorsoventral flattening of the rib cage and bowing of the

proximal end of the tibia (Breves and Schröder, 1991).

B-Histology:

Histological differentiation of the type of rickets from an early case is

by no means as clear cut as would appear from the above descriptions of

more advanced changes. However examination of undecalcified

histological sections stained for calcium allows one to diagnose rickets

with confidence even though the type may not be clear. Rickets occurs

most commonly in very early life when skeletal growth is most rapid,

usually from 2 to 3 weeks of age (MacDonald,1995).

C-Techniques to Measure Bone Mineral

There are two widely utilized techniques to assess bone mass. They

variously assess mineral content of regional sites particularly those sites

at risk of osteoporotic fracture such as the wrist, spine and hip, but also

the whole skeleton (MacDonald,1995).

Treatment of vitamin D deficiency

It has been found that the feeding of chickens a single massive dose of

15,000 IU vitamin D3 cured rachi c chicks more promptly than when

generous levels of the vitamin were added to feed. This single oral dose

protected cockerels against rickets for 8 weeks and pullet chicks for 5

weeks. In giving massive doses to rachitic chicks, it should be

remembered that excess vitamin D can be harmful. The dose should be

scaled to the degree of deficiency, and excessive amounts of vitamin D

should not be added to feed ( Jianhua et al.,2000).

2.1.3. Vitamin E deficiency and selenium deficiency

Vitamin E is required for normal embryonic development in chicken.

Vitamin E is a very effective antioxidant. It is an important protector in

feeds of the essential fatty acids and other highly unsaturated fatty acids

as well as vitamins A and D3, carotenes, and xanthophylls (Puls, 1994).

Vitamin E deficiency produces encephalomalacia, exudative diathesis,

and nutritional myopathy (muscular dystrophy) in chicks. Vitamin E

plays multiple roles in poultry nutrition. It is required not only for normal

reproduction and for most effective antioxidant for prevention of

encephalomalacia, in a specific role interrelated with action of selenium

has been shown to be an essential mineral element for both chicks and

poults. It is a constituent of the enzymes, glutathione peroxidase and

phospholipid hydroperoxide glutathione peroxidase, which serve to

protect tissues against oxidative damage, and it is a component of

iodothyronine 5’-deiodinase, an enzyme that is involved in the

conversion of thyroxine to its active form (Guesry, 1998).

Clinical Signs

Puls,(1994) show the encephalomalacia in chicks is a nervous

syndrome characterized by ataxia or paresis . Forced movements،

increasing incoordination, rapid contraction and relaxation of the legs,

and finally complete prostration and death. Even under these

conditions, complete paralysis of legs is not observed .

Postmortem lesion

No have been abserved lesion in leg and histopatholocal examination

degenerative neuronal changes occur everywhere but are most

prominent in Purkinje cells and in large motor nuclei. Ischemic cell

change is most frequently encountered. Peripheral chromatolysis with

the Nissl substance packed along the periphery of the cell nucleus is also

common (Scherer and Baker ,2000).

Diagnosis

Signs, lesions, feed rancidity, histopathology,response to medication

(Scherer and Baker ,2000).

Differential diagnosis

Newcastle disease (nervous form) encephalitis ,Rickets ,vitamin A

deficiency, Riboflavin deficiency ,perosis, encephalomyelitis, toxicities

and necrotic dermatitis can be differentiated from vitamin E deficiency

by histologic examination of the brain (Scherer and Baker ,2000).

Treatment of Deficiency.

Vitamin E and/or selenium in feed and/or water. Broad-spectrum

antibiotics where there are extensive skin lesions. Encephalomalacia

may or may not respond to treatment with vitamin E, depending on the

extent of damage to the cerebellum (Hulland, 1993).

Prevention

Proper levels of vitamin E, selenium, antioxidant, good quality raw

material ( Hulland, 1993).

2.1.4. Thiamine (Vitamin B1) deficincy

Thiamine is converted in the body to an active form, thiamine

pyrophosphate, which is an important cofactor in oxidative

decarboxylation reactions and aldehyde exchanges in carbohydrate

metabolism. Deficiency of thiamine leads to extreme anorexia,

polyneuritis, and death (Chiang et al.,1997).

Pathophysology and pathology

The metabolically action form of thiamine ,which is called thiamine

pyrophosphate(TPP),is involved in the intermediary metabolism of

carbohydrates.Thiamine pyrophosphate is involved with the three

enzymes ystem.(a)pyruvate dehydrogenase, which converts pyruvate to

acetyl coenzyme A; (b)α-ketoglutarate dehydrogenase which convert α-

ketoglutarate to succinate in kerbs cycle;and (c)transketolase,which

catalyzes the pentose monophosphate shunt (Guesry, 1998).

Thiamine pyrophosphate deficiency lead to elevated level of serum

pyruvate and occasionally lactate reduced red blood cell transketolase

activity and decrease in oxygen uptake and transketoiase activity in the

brainstem .The requirement for thiamine is greatest during period of

high metabolic demand. Thiamine deficiency causes peripheral

neuropathy.The primary changes in the perpherial nerves is segmental

demyelination associated with axonal degeneration which is most

marked in the distal portion of the peripheral nerves (Guesry, 1998).

Clinical Signs

In young chicks, it may appear before 2 weeks of age. leg weakness,

and an unsteady gait. Adult chickens often show as the deficiency

progresses, apparent paralysis of muscles occurs beginning with the

flexors of the toes and progressing upward affecting the extensor

muscles of legs. The chicken characteristically sits on its flexed legs and

draws back the head in a “stargazing” position.The chicken soon loses

the ability to stand or sit upright, and it topples to the floor where it

may lie with the head still retracted (Chiang et al.,1997).

Diagnosis

Based on clinical signs history of nutritional deficiency and serum

thiamine levels is of limited usefulness because the level dose not

reliably reflect ssue concentra on (Guesry,1998).

Treatment

Chickens suffering from thiamin deficiency respond in a matter of a

few hours to oral administration of the vitamin. Because thiamin

deficiency causes extreme anorexia, supplementing feed with the

vitamin is not a reliable treatment until after chickens have recovered

from acute deficiency, should be the ration contaent 1.5 gm/tone

(Johnson et al.,2000).

2.1.5. Riboflavin (Vitamin B2)

Riboflavin is a cofactor in many enzyme systems in the body. Examples

of riboflavin-containing enzymes are Nicotenamid Adenine

Dinucleotid(NAD) and Nicotenamid Adenine Dinucleotid-Phosphate

(NADP)-cytochrome reductases, succinic dehydrogenase, acyl

dehydrogenase, diaphorase, xanthine oxidase, L- and D-amino acid

oxidases, L-hydroxy acid oxidases and histaminase, some of which are

vitally associated with oxidation-reduction reactions involved in cell

respiration. Riboflavin deficiency is most commonly reported in

chickens. Deficiency of riboflavin in chickens can cause peripheral

neuropathy, resulting in a condition called "curled-toe paralysis (Guesry,

1998).

Pathogensis

In cases of curled-toe paralysis, degeneration of the neuromuscular

end plate and muscle tissues is often found. Riboflavin is probably also

essential for myelin metabolism of the main peripheral nerve trunks. No

gross dystrophy develops، although muscle fibers are in some cases

completely degenerated. The sciatic nerve exhibits myelin degeneration

in one or more branches. Similar changes are apparent in the brachial

nerve trunks (Scherer and Baker,2000).

Clinical Signs

When chicks are fed a diet deficient in riboflavin، they grow very slowly

and chicks do not walk except when forced to do so and then they

frequently walk on their hocks. Leg paralysis may be more prevalent

than curled toe paralysis. Toes are curled inward when both walking and

resting . Young chicks in advanced stages of deficiency do not move

around and splayed legs (Puls, 1994).

Postmortem lesion

In severe cases of riboflavin deficiency, chicks show marked swelling

and softening of sciatic nerves usually undergo the most pronounced

changes, some mes reaching a diameter 4—5 mes normal size. Leg

muscles are atrophied and flabby and the skin is dry and harsh.

Histologic examination of affecte nerves shows degenerative changes in

myelin sheaths of the main peripheral nerve trunks.This may be

accompanied by axis cylinder swelling and fragmentation (Chiang et

al.,1997).

Differential diagnosis

The differential diagnosis includes a vitaminosis A, avian

encephalomyelitis (epidemic tremor), thiamine and pyridoxine

deficiencies (Anon,2006).

Diagnosis

Diagnosis is depended on sgns, lesion and microscopic examination of

the peripheral nerves revealed axonal degeneration, interstitial edema,

proliferation of mononuclear cells and infiltration of lymphocytes

(Scherer and Baker,2000).

Treatment

Two 100-µg doses of riboflavin should be sufficient for treatment of

riboflavin-deficient chicks, followed by incorporation of an adequate

level in the ration. When the curled-toe deformity is of long standing,

however, irreparable damage has occurred and administration of

riboflavin no longer cures the condition (Johnson et al.,2000).

2.1.6. Gout

There are tow types of gout

Visceral Gout : A condition in which white uric acid or uratecrystals

deposits are seen in soft tissues of various organs in body.

Articular gout : Conditions in which urate crystals deposit are seen in

joints ( Chio et al.,2004).

Articular Gout

Gout is the most familiar example of an arthritis-related disease linked

with diet. When an excess of uric acid remains in the body — because

too much is produced or very little is excreted — it can deposit

microscopic crystals in the joints ( Chio et al.,2004) . Articular gout is

characterized by the accumulation of urates in the synovial capsule and

tendon sheath of a joint. This causes inflammation of the joint lining and

considerable pain. It is rare or sporadic (Styles and Phalen,1998).

Causess of Articuler Gout

a. Genetics.

b. High protein in the diet.

c. High calcium diet with low phosphorous results in precipitation of

calcium sodium urate crystals. In addition excessive use of Sodium

bicarbonate or excessive sodium, low vitamin A diet, high protein diet

(30%) and water depriva on due to any reason leads to concentra on of

uric acid and other minerals in the blood and later in the kidney. Hard

water with higher metallic salts favors the condition and puts extra load

on kidneys (Styles and Phalen,1998).

Pathogensis

It is probably due to a metabolic defect in the secretion of urates by the

kidney tubules (Lee et al.,2004).

Clinical signs

Clinical signs of articular gout may include reluctance to move, shifting

from leg to leg, lameness, and joint swelling (Lierz,2003).

Postmortem lesion

Soft tissues around the joints are always involved, especially feet.

Other joints of the legs, is commonly involved. Soft tissues other than

synovium are rarely involved (Lierz,2003).Microscopic Lesion

Granulomatous inflammation in synovium and other tissues

(Varalakshmi et al.,1990).

Diagnosis of Gout

Visceral gout is most often seen during a necropsy and is difficult to

diagnose in a living specimen. The most frequently seen sign of the

disease is sudden death. The symptoms,are vague and non-specific and

can include depression, lethargy anorexia, feather plucking or other

behavioral changes. Absent definitive symptoms, uric acid levels can be

routinely monitored. If the levels become elevated, an endoscopic

procedure can be diagnose gout (Lee et al.,2004).Cytologic evalua on of

gouty lesions reveals uric acid crystals and inflammatory cells

(Lierz,2003).

Treatment and Prevention or Control

1-At hatchery level try to minimize dehydration at all stages including

chick holding and transport etc.

2-Make sure that the chicks get free and ample access to drinking water.

Maintain water temperature to room temperature. Adjust proper height

of drinkers. In case of nipple drinking system use water cups for few days

or water fonts. Maintain correct temperature at litter level during arrival

of chicks and first 10 days at-least. Try to maintain 60 % plus or 70%

humidity during first3 days of chick life. Allow chicks to drink water for 1

or 2 hours and then only offer pre-starter feed (Lee et al.,2004).

3-Ensure correct level of calcium and phosphorous levels in feed. Use

toxin binders and liver tonics to keep minimum levels of fungal toxins in

feed. Avoid excessive protein levels in diet over suggested .

4-Use recommended levels of aluminum-free Sodium bicarbonate

(baking soda) in feed during high temperatures (Lee et al .,1994)

Varalakshmi et al.,1990).

2.2- Bacterial Diseases :

2.2.1- Colibacillosis :

Definitions and Synonyms

Colibacillosis refers to any localized or systemic infection bcaused

entirely or partly by avian pathogenic Escherichia coli (APEC) including

colisepticemia, coligranuloma (Hjarre’s disease), air sacculitis, chronic

respiratory disease (CRD), cellulitis , swollen-head syndrome, peritonitis,

salpingitis, osteomyelitis/synovitis,panophthalmitis, omphalitis and yolk

sac infec on (Barnes, 2000).

Etiology

Esherichia coli (E coli) strains beiong to to coliform group of

microorganisms which are a common part of the normal facultative

anaerobic microflora of the intestinal tract of most bird including

chickens Gram negative,non-sporeforming, rod shaped bacterial which

ferment lactose, Oxidose negative,catalase positive ( Aggad et al., 2010)

.

Classification

Escherichia coli classification

Phylum:Proteobacteria

Class:Gamma proteobacteria

Family:Enterobacteriacae

Genouse:Esherichia

Species:coli

According to (Be elheim, 1994).

Transmission

E. coli is present in the intestinal tracts of most animals and shed in

the faece, often in high numbers. Direct or indirect contact with other

animals faeces can introduce new strains into the poultry flock. Free-

living birds are especially important as they are colonized with strains

that are already adapted to avian species ( Fallacara et al ., 2001).

Signs

Hammodi and Aggad ,( 2008) refer to the chickens affected by

necrotic dermatitis and characterized by a chronic inflammation of the

subcutis of thighs . Septicemia occasionally also leads to synovitis and

osteomyelitis (Lutful Kabir,2010) . In poultry E coli infections may cause

inflammation of the joints which can lead to lameness ( Jacob et al

.,2003).

Postmortem lesion

Lesions are often extensive and severe in birds that survive into the

second weeks. Occasionally chickens with advanced tenosynovitis,

arthritis involving the hock joint and flexor tendons may be found late in

the disease (Huff et al.,2001). The most common lesions associated with

colibacillosis are osteomyelitis , arthritis may be encountered ( Dziva and

Stevens , 2008). Localization of E. coli in bones and synovial tissues is a

common sequel to colisepticemia. The term osteoarthritis is used when a

joint is inflamed, one or more bones have osteomyelitis. Polyarthritis

refers to the involvement of more than one joint (McNamee and Smyth,

2000 ; Al Ankari et al., 2001).

Figure (1).Advanced tenosynovitis,arthritis involving the hock joint and flexor tendons

Diagnosis

Isolation and Identification of Causative Agent diagnosis is based on

the isolation and identification of E. coli from lesions typical of

colibacillosis. Care must be taken to avoid fecal contamination of

samples. Isolation of the organism from visceral organs of birds

undergoing decomposition must be interpreted cautiously as E. coli

rapidly spreads from the intestinal tract of dead birds. Bone marrow

cultures are easy to obtain and are generally free of contaminating

bacteria (Lee and Arp, 1998).

Differential Diagnosis

Many other organisms including viruses, mycoplasmas, and other

bacteria can cause synovial lesions similar tothose resulting from E. coli

infection (Al Ankari et al., 2001).

Treatment and prevention

E.coli may be sensitive to many drugs such as ampicillin,

chloramphenicol, chlortetracycline, neomycin, nitrofurans, gentamicin,

ormethiprim-sulfadimethoxine, nalidixic acid, oxytetracycline,

polymyxin B, spectinomycin, streptomycin, and sulfa drugs. Water

administration of apramycin proved effective in reducing the numbers of

organisms in the digestive tract and preventing bacteremia in chickens (

Leitner et al., 2001). In most cases, symptomatic treatment (fluids,

antidiarrheals) is all that is required. In more severe infections, antibiotics

such as tetrac ycline and chloramphenicol may be necessary ( Jacob et

al.,2003).

2.2.2- Mycoplasma Synoviae infection Mycoplasma synoviae infection most frequently occurs as a

subclinical upper respiratory infection and is sometimes responsible for

infectious synovitis in broilers (Gautier-Bouchardon et al., 2002).

Mycoplasma synoiae (MS) becomes systemic and results in infectious

synovitis, an acute to chronic infectious disease of chickens involving

primarily the synovial membranes of joints and tendon sheaths producing

an exudative synovitis

( Ley et al., 1997).

Etiology

Mycoplasma spp differ from other bacteria in their very small size and

absence of a cell wall these characteristics account for their “fried egg”

type of colonial morphology, complete resistance to antibiotics such as

pencilline that affect cell wall synthesis (Kleven, 1997). Mycoplasma

colonies were observed as satellites adjacent to Micrococcus colonies

(Fan et al.,1995).

Transmission

Vertical transmission occurs in naturally and artificially infected

chickens. vertical transmission plays a major role in spread of MS in

chickens. Lateral transmission occurs readily by direct contact ( Kleven,

1997).

Clinical signs Mycoplasma synoviae may cause either respiratory disease or

infectious synovitis (Branton et al.,1999). The first observable signs in a

flock affected with infectious synovitis are lameness, and retarded

growth. Swellings usually occur around joints ( Morrow et al., 1997).

Hock joints and foot pads are principally involved, but in some birds

most joints are affected; however, birds occasionally are found with a

generalized infection but not with apparent swelling of the joints (Salisch

al et., 1998). Morbidity in chickens with clinical synovitis varies from

2—75%, with 5—15% being most usual and Mortality is usually less

than 1%, ranging up to 10% (Christensen et al .,1994).

Gross lesion

Chickens. In early stages of the infectious synovitis for the disease,

chickens frequently have a viscous creamy to gray exudate involving

synovial membranes of the tendon sheaths,and joints, as the disease

progresses. Caseous exudate may be found involving tendon sheaths,

joints (Tiong ,1990).Articular surfaces, particularly of the hock and

shoulder joints, become variably thinned to pitted over time

(Noormohammadi et al., 1997).

The histopathology of infectious synovitis in chickens caused by M.

synoviae has been described the joints, particularly of the foot and hock,

have an infiltrate of heterophils (phagocytosis) and fibrin into joint

spaces and along tendon sheaths (Bradbury, 1994). The synovial

membranes are hyperplastic with villous formation and a diffuse to

nodular subsynovial infiltrate of lymphocytes and macrophages (Branton

et al,1999)

Diagnosis

Prosumative diagnosis based on history,signs,and

lesion.Positive diagnosis may be made by isolation and identification of

M synoviae. Isolation from lesions in acutely infected birds is not

difficult, but in the chronic stages of infection, viable organisms may be

no longer present in lesions.( Bencina et al., 1994). Serological tests are

also widely used for diagnosis and can be detected by ELISA

(Gross,1990).

Differential diagnosis Staphylococcal arthritis can also cause swollen joints with a creamy

exudate sometimes extending into the tendon sheaths. Reovirus infection

can also cause swelling of joints and tendon sheaths, but the exudate is

more watery or bloodtinged, unless secondary Staphylococcal infections

occur. (Garcia et al., 1994).

Treatment and control

Tylosin is adrug of choise for treatment Mycoplasma synoviae.

Vaccinnation with inactivation oil emulsion vaccine . Dose 0.5 ml s/c age

6-8 weeks this vaccine dose not prevention and infection but decrease

signs (chin et al.,1991).

2.2.3- Pullorum disease

Infections with Salmonella pullorum can result in acute systemic

disease and a high incidence of mortality in young poultry

(Snoeyenbos, 1991; Salem et al.,1992). The disease had been previously

known as bacillary white diarrhae ,but as white diarrhea was not always

a clinical feature it became better known as pullorum disease (pattison

et al.,2008).

Etiology

Salmonella pullorum is non motile ,gram negative (Rober and port, 1998

; Pattison et al, 2008; Ritchard et al,1997).

Transmission

Can be transmited in several ways (Anon, 2008)

Bird-to-bird contact

Hen to egg to chick (recovered hens will pass on the disease to

roughly 1/3 of her eggs)

Chick to chick

Cannibalism of infected carcasses

Wound contamination

Fecal contamination of feed, water and litter

Clinical signs

Pullorum disease is most lethal in young birds at 3 weeks old or less

with minimal affects on adults is show lameness (Ashton, 1990 ; Jindal

et al .,1999 ; Pa son et al .,2008 ; Ritchard et al ., 1997; Pomeroy and

Nagaraja, 1991).

Gross lesion

Chicks:

The hock joint is most commonly involved ,but other joint such as the

wing joint and the foot pad they may also swollen (Ritchard et

al,1997).In growers affected with arthri s, the hock joint is usually

enlarged because of the presence of excess lemon-or orange-coloured

gelatinous material around the joint (Pattison et al., 2008; Barrow,

1992).

Adult chicken

Pattison et al.,( 2008) Show the swollen containing yellow viscous fluid

, Swollen joints, most commonly the hock, which contain yellow

fibrinous fluid. Lesions is Arthritis (Ashton, 1990).

Diagnosis

A definitive diagnosis of (PD) requires the isolation and identification

of S. pullorum. A tentative diagnosis, however, can be made based on

history, clinical signs, mortality, and lesions (Gast and Holt, 1998).

Differential diagnosis

S. pullorum can localize in major joints and tendon sheaths of chicks

Such signs and lesions resemble those produced by organisms such as

Mycoplasma synoviae, Staphylococcus aureus, Pasteurella multocida (

Gast and Beard, 1990).

Tretment

Therapeutic drugs such as, nitrofurans, chloramphenicol, tetracyclines,

and aminoglycosides have been found to be effective in reducing

mortality from PD. The Sulfonamides that have been used in the

treatment of PD sulfadiazine, sulfamerazine, sulfathiazole,

sulfamethazine, and sulfaquinoxaline ( Aziz et al., 1997).

Prevention and Control

Vaccines to control PD. killed bacterin is produced in th United States,

and live modified vaccines used in other countries are not permitted in

the United States (Barrow et al., 2000).

2.2.4- Fowl Typhoid

Fowl typhoid(FT) caused by S gallinarum, is an acute septicemiam or

chronic disease of domesticated adult bird mainly chickens.These

microorganisms cause systemic disease in a wide range of domestic

poultry, including chickens (Anon, 1994).Causing heavy mortality in

chickens (Pattison et al.,2008).

Eteiology

Salmonella Gallinarum is Gram negative (Ritchard et al.,1997;

Pattison et al.,2008).

Transmission

Birds may infect not only by horizontal transmission, but also

succeeding ones through egg transmission. Egg transmission may result

from contamination of the ovum following ovulation but localization of S

gallinarum in the ovules before ovulation is likely and probably

constitutes the chief mode of vertical transmission( Barrow,1992 ; Islam,

2003).

Clinical signs

Lameness with swollen hock joints and poor growth rate may be seen

in subacute form in growing chicks ( Jindal et al., 1999).

Gross lesion

Some birds may exhibit swollen joints containing yellow viscous fluid.

Among the joints the hock joint is most commonly involved but, other

joints such as the wing joint and the foot pad may be affected

(Pennycott and Duncan, 1999).

Diagnosis

A tentative diagnosis of fowl typhoid disease can be made on flock

history, clinical signs and post mortem lesions (Samad, 2005 ; Gast and

Beard,1990 and Snoeyenbos, 1991).

Differential Diagnosis

Lesions of (FT) resemble those produced by organisms such as

Mycoplasma synoviae, Staphylococcus aureus, Pasteurella multocida.

Sometimes the white nodules in the heart of young chicks may resemble

Marek’s disease . Local infections with S. gallinarum in adult carriers,

particularly of the ovary, may appear identical to those produced by

other bacterial infections such as coliforms, P. multocida, streptococci,

and other salmonellae ( Gast and Beard, 1998).

Treatment

A number of antibacterial agents reduce the morbidity and mortality

of used to treat birds infected of fowl typhoid. Supply of 0.04%

furazolidone in feed for consecu ve 10 days is generally considered to

be the best treatment. (Khan et al., 2005; Islam, 2003)

Prevention and control

Vaccine was developed that used successfully in many flock. It was a

live attenuated rough strain of S. gallinarum known as vaccine 9R.A er

subcutaneous injec on into chicken between 10and 18 weeks of age it

usually gave solid , long-lasting immunity.vaccination reduces mortality

in flock challenged with S.gallinarum and dose not depress egg

production when used in flock free of the disease ( Pattison et al., 2008).

2.2.5- Botulism

Botulism is an intoxication caused by exotoxin of Clostridium

botulinum. Synonyms are “limberneck” and “Western duck sickness.”

Free-ranging and confinement-reared poultry and feral birds can be

affected. Most avian cases are caused by C. botulinum type C, although

outbreaks due to other toxin types have been described ( Dohms, 1987).

The public health significance of avian type C botulism outbreaks is

considered minimal (Jensen and Price,1987).

Etiology

Clostridium. botulinum is a gram-positive, spore-forming bacterium

capable of elaborating potent exotoxins under appropriate environmental

conditions( Mitchell and Rosendal, 1987). The species consists of a

diverse group of anaerobic bacteria including 4 cultural (I—IV) and 8

antigenically different toxigenic groupings (A, B, C alpha, C beta, D, E,

F, and G). Human disease has been associated mainly with types A, B, E,

and F, and A, C, and E have caused disease in birds (Smith et al., 1975).

Cases of botulism in chickens in natural or commercial settings have been

caused primarily by the type C toxigenic group ( Smart et al.,1987).

Incubation Period

Morbidity and mortality were dose related with high levels of toxin,

disease appears within hours while with low toxin doses, onset of

paralysis occurs within 1—2 days (Jeffery et al.,1994).

Transmission

Clostridium botulinum type C is distributed worldwide wherever

large populations domestic birds are found. Type C organisms readily

grow in the gastrointestinal tract of birds and are considered obligate

parasites Type C spores commonly are found in and around poultry .

Presence of organisms in the gastrointestinal tract of wild and domestic

birds and resistance of spores to inactivation, favor spread of this

organism (Jensen and Price, 1987).

Morbidity and Mortality

Morbidity and mortality are related to the amount of acquired toxin.

Low levels of intoxication produce little mortality and morbidity, which

can confuse diagnosis. In severe cases, up to 40% mortality has been

observed in broiler flocks (Dohms, 1987)

Signs

Clinical signs of botulism in chickens, flaccid paralysis of legs, wings,

neck, and eyelids are predominant features of the disease. Paralytic signs

progress cranially from the legs to include wings, neck, and eyelids.

Initially, affected birds are found sitting and are reluctant to move

(Bohnel , 2002). If coaxed to walk, they appear lame. Wings droop when

paralyzed. Limberneck, the original and common name for botulism,

precisely describes the paralysis of the neck (Jeffery et al.,1994).

Postmortem lesion

Possibly no significant lesions. Mild enteritis if has been affected for

some time. Feathers may be easily pulled (chicken only). Maggots or

putrid ingesta may be found in the crop (Jeffery et al.,1994).

Diagnosis

The differential diagnosis of botulism is based on clinical signs and

lack of gross or microscopic lesions. Definitive diagnosis requires

detection of toxin in serum, crop, or gastrointestinal washings from

morbid birds .Serum is the preferred diagnostic sample. Because C.

botulinum is found in the gut of normal chickens, toxin can be produced

in decaying body tissues. Therefore, finding toxin in tissues of dead birds

does not confirm botulism. The mouse bioassay is a sensitive and reliable

method for confirming heat-labile toxin in serum ( Dohms, 1987).

An antigen-capture ELISA assay for C. botulinum type C toxin was

able to detect 0.25ng/ml toxin compared to 0.12ng/ml detection using the

mouse bioassay. However, using larger sample volumes in ELISA proved

to be as sensitive to the mouse test due to the concentrating effect of the

capture antibody (Rock et a1.,1998).

Treatment

Treatment of affected broiler flocks with sodium selenite and vitamins

A, D3, and E reduced mortality (Notermans et al. 1980). Antibiotics

including bacitracin (100 g/ton in feed), streptomycin g/L in water), or

periodic chlortetracycline treatments also reduced mortality. Penicillin

was ineffective in controlling one outbreak but has been found

efficacious in other affected flocks. In vitro susceptibility of C. botulinum

to 13 antibiotics was reviewed (Facile et al. 2000).

2.2.6- Staphylococcosis

Bumblefoot, also known as plantar pododermatitis, is a common

disorder of maturing males of the heavy breeds. Bumblefoot is

characterized by lameness, swelling, heat, reluctance to walk, and a hard,

pus-filled abscess on the pad of the foot covered by a black scab.

Bumblefoot results from injury or abrasion to the lower surface of the

foot, which allows for the introduction of staphylococcus bacteria.

Lesions can occur on toes, hocks and the pads of the feet. Bumblefoot is a

chronic disease that if left untreated can result in a 50 percent mortality

rate (Cotter and Taylor,1999).

Eteoilogy

Staphylococcus aurous are Gram positive ,aerobic or faculitative

anaerobic, oxidase negative, catalase positive and fermentive of the

mannatol (Capita et al.,2001 ; Wilcox et al., 2009).

Clinical signs

Chronic inflammation characterized clinically by ulceration, and

swelling of the plantar metatarsal or digital pads, or both, in birds.

Bumble foot causes pain, impedes perching and walking.Laminess (

Wilcox et al.,2009 ).

Postmortem lesion

Bumble foot will compromise the internal tissues of the foot, such as

the mesoderm, tendons and bones, causing osteomyelitis, synovitis,

laminitis

(Golden and Brown,1991).

Diagnosis

Isolation and Identification of Causative Agent S. aureus is diagnosed

by culturing suspected clinical material including exudate from joints,

( Pezzlo, 1992 ; collee et al.,1996)

Treatment

Treatment include penicillin, streptomycin, tetracyclines,

erythromycin, novobiocin, sulfonamides, lincomycin, and spectinomycin

(Richard,1997 )

CONCLUSIONS

AND

RECOMMENDATIONS

Conclusion

1-The legs paralysis sign is a significant sign for many bacterial and

nutritional diseases .

2- The legs paralysis was mainly due to histological changes which was

obviously seen .

3- Determined some of the bacterial and nutritional diseases that cause

the leg paralysis.

Recommendation

1-Study the bacteriological and nutritional cause of legs paralysis

2-Produce vitamin rich ration

3-Chicks which suffering from legs paralysis must be diagnosed and eradicated

4-Study the legs paralysis cases serologically and find the relationship between this case and neural disorder

REFERENCES

Reference

(Anon, 2006)http://www.ivis.org/advances/Kearns/kearns2/ivis.pdf.

(Anonyms, 2008)http://extension.unh.edu/Agric/AGDLEP.htm

Aggad, H.;Ammar, Y.A .; Hammoudi, A. and Kihal, M. (2010).

Antimicrobial resistance of Escherichia coli Isolated from chickens with

colibacillosis. J.Global Veterinaria. 4(3): 303-306.

Al Ankari, A. R.; Naylor, J. M.; Worthington, K. J.; Payne Johnson, C.

and Jones, R. C. (2001). Avian pneumovirus infection in broiler chicks

inoculated with Escherichia coli at different time intervals.J. Avian

Pathol. 30:257-267.

Alzubaidi, S.S. (1986). Poultry Management. College of Agricultural, Basra,

University P:3.

Ameenuddin, S.; Sunde, M. L. and Cook, M. E. (1985). Essentiality of

vitamin D3 and its metabolites in poultry nutrition: a review. J. World

Poult. Sc.. 41:52-63.

Anon,(1994). The national poultry improvement plan an auxiliary provisions.

United States Department of Agriculture, Animal Plant Health Inspection

Service. Hyattsville, MD.78-79

Arora, A. K.; Sandhu, K. S. and Sodhi, S. S. ( 1998). Comparativ studies on

efficacy of different vaccines against fowl typhoid in chickens. J. Ani.

Sci. 68:297-299.

Ashton, W.L. (1990). Enterobacteriaceae. In: Poultry Diseases. 3rd ed. Jordan,

F.T.W. (ed). BalliereTindall, Philadelphia, Pp: 11–41.

Aziz, N. S.; Satija. K. C., and Garg, D. N. (1997). The efficacy of gentamicin

for the control of egg-borne transmission of Salmonella gallinarum. J.

Indian Vet. 74:731-733.

Baksh, I. (1994). Permaculture for poultry.J. Farming /February, Pp: 13-14

Balnave, D. (2004) .Challenges of accurately defining the nutrient requirements

of heat-stressed poultry.J. Poult. Sci. 83:5-14.

Ban, Y. (2000). Vitamin D receptor gene polymorphism is associated with

Graves’ disease in the Japanese population. J.Clinical Endocrinology and

Metabolism. 85: 4639-4643.

Barnes, H. J. (2000). Pathological manifestation of colibacillosis in poultry.

Proc 21st World’s Poultry Congress, Montréal, Canada, Aug 20-24.

Barrow, P. A. (1992). In-vitro and in-vivo characteristics of TnphoA mutant

strains of Salmonella gallinarum serotype not invasive for tissue culture

cells. J. Med. Microbiol. 36:389-397.

Barrow, P. A.; Lowell, M. A. and Stocker, B. A.( 2000). Protection against

experimental fowl typhoid by parenteral administration of live SL5828,

an aroA-serC (aromatic dependent) mutant of a wild-type Salmonella

Gallinarum strain made lysogenic for P22 sie.J. Avian Pathol. 29:423-

431.

Barrow, P.A. (1992).Further observations on the serological response to

experimental Salmonella typhimurium in chickens measured by ELISA.

.J.Epidemiol. Infect. 108: 231-241.

Bartholomew, A.; Latshaw, D. and Swayne, D. E. (1998). Changes in blood

chemistry, hematology, and histology caused by a selenium/vitamin E

deficiency and recovery in chicks.J. Biol. Trace Elem. Res. 62:7-16.

Bencina, D.; Kleven, S. H.; Elfaki, M.; Snoj, A. P.; Dorrer-Dovc, D. and

Russ, I.( 1994). Variable expression of epitopes on surface of

Mycoplasma gallisepticum demonstrated with monoclonal antibodies.J.

Avian Pathol. 23:19-30.

Bencina, D.; Tadina, T. and Dorrer, D. (1988). Natural infection of ducks

with Mycoplasma synoviae and Mycoplasma gallisepticum and

mycoplasma egg transmission.J. Avian Pathol. 17:441-449.

Bettelheim, K. A. (1994). Biochemical characteristics of Escherichia coli. In

Escherichia coli in Domestic Animals. Gyles, C. L. (Editiors=.).4thEd,

Wallingford,UK, Pp: 3-30.

Bhattacharyya, H. M.; Chakraborty; G. C.; Chakraborty, D.;

Bhattacharyya, D. ; Goswami, U.N. and Chatterjee, A. (1984). Broiler

chick mortality due to pullorum disease and brooder pneumonia in West

Bengal. Indian J. Anim. Hlth.23:85–88.

Bisgaard, M. (2004): In vivo studies of Gallibacterium anatis infection in

chickens.J. Avian Pathol. 33(2): 145-152.

Bohnel, H. (2002) Household biowaste containers (bio-bins) – potential

incubators for Clostridium botulinum and botulinum neurotoxins. Water,

Air, and Soil Pollution. J.Poul. Sci. 140(4):335-341.

Bradbury, J. M.; Yavari, C. A. and Giles, C. J. ( 1994). In vitro evaluation of

various antimicrobials against Mycoplasma gallisepticum and

Mycoplasma synoviae by the microbroth method, and comparison with a

commercially-prepared test system. J.Avian Pathol. 23:105-115.

Branton, S. L.; Lott, B. D.; May, J. D.; Maslin, W. R.; Pharr, G. T.; Brown,

J. E. and Boykin, D. L. (1999). The effects of (F) strain Mycoplasma

gallisepticum, Mycoplasma synoviae, and the dual infection in

commercial layer hens over a 44- week laying cycle when challenged

before beginning of lay. II. Egg size distribution.J. Avian Dis. 43:326-

330.

Breves, G. and Schroder, B. (1991). Comparative aspects of gastrointestinal

phosphorus metabolism. J.Nutr. Res. Rev. 4:125-140.

Byrd, J. A.; DeLoach J. R.; Corrier, D. E.; Nisbet, D. J.; and Stanker, L. H.

(1999). Evaluation of Salmonella serotype distributions from commercial

broiler hatcheries and grower houses.J. Avian Dis. 43:39-47.

Capita, R.; Alonso-Calleja C. ; Garcia-Fernandez . M. C, and Moreno, B.

(2001). Processing and products characterization of Staphylococcus

aureus isolated from poultry meat in Spain. J. Microbiology. 39(3): 219-

225.

Chen, B. J.; Shen, T. F.; and Austic, R. E. (1996). Efficiency of tryptophan-

niacin conversion in chickens and ducks. Nutr. Res. 16:91-104.

Chiang, Y. H.; Kim, J. D.; Lee, C. S. and Holick. F. M. (1997). Biological,

biochemical and histopathological observations of broiler chicks fed

different levels of vitamin D-3. III: Histopathological observation.

Korean .J An. Nutr. Feedstuffs. 21:245-250.

Chin, R. P.; Meteyer, C. U.; Yamamoto, R.; Shivaprasad, H. L. and Klein,

P. N. (1991). Isolation of Mycoplasma synoviae from the brains of

commercial meat turkeys with meningeal vasculitis. J.Avian Dis. 35:631-

637.

Chio, H. H.; Atkin, K.; Karlson, E.W.; Willett, W. and Curhan, G. (2004).

Purine-Rich Foods, Dairy and Protein Intake, and the Risk of Gout in

Men. J.New England Medicine. 350(11):1093-1103

Christensen, N. H.; Yavari, C. A.; McBain, A. J. and Bradbury, J. M.

(1994). Investigations into the survival of Mycoplasma gallisepticum,

Mycoplasma synoviae and Mycoplasma iowae on materials found in the

poultry house environment.J. Avian Patho. 23:127-143.

Chung, J. Y.; Wilkie, I.; Boyce, J. D. and Adler, B. (2005). Vaccination

against fowl cholera with acapsular P. multocida A: J.Vaccine, 23 (21):

2751- 2755.

Chung, J.Y.; Wilkie, I.; Boyce, J.; Kirsty, M.; Alanj ,T . F ; Ghggousi, M .;

and Ben Adler. D. (2001) . Role of Capsule in the Pathogenesis of Fowl

Cholera Caused by Pasteurella multocida Serogroup A. J. Infection and

Immunty. 69(4). 2487-2496.

Collee, J. G.; Fraser, A. C.; Marmion, B. P. and Simmons, A. (1996).

Practical medical microbiology. 14thEd. , Melbourne Charchill

Livingstone.New York, Pp:389-396

Cotter, P. F. and Taylor, R. L. (1999). Differential resistance to

Staphylococcus aureus challenge in two related lines of chickens.J. Poult.

Sci.70:1357-1361.

Daghir, N. J. (2009). Nutritional Stratigies to Reduce Heat Stress in Broilers

and Broiler Breeder.J. Lohmann Information.44(1):6.

Davies, R. (2004). Fowl typhoid and Pullorum disease. In Manual of

Diagnostic Tests and Vaccines for Terrestrial Animals. 5th ed.,

OIE.Pp:83-86

Dohms, J. E. (1987). Laboratory investigation of botulism in poultry. In: Avian

Botulism: An International Perspective. Eklund, M. W. and Dowell, V.

R. Charles C. Thomas(Editiors.).: Springfield, IL,UK.Pp: 295-314.

Dziva , F . and Stevens , M . P. (2008). Colibacillosis in poultry: unraveling

the molecular basis of virulence of avian pathogenic Escherichia coli in

their natural hosts. J.Avian Pathol. 37(4): 355-366.

Edwards, H. M.; Elliot, M. A.; Sooncharernying, S. and Britton, W. M.

(1994). Quantitative requirement for cholecalciferol in the absence of

ultraviolet light. J.Poult. Sci. 73:288-294.

Erbeck, D. H., McLaughlin, B. G. and Singh, S. N. ( 1993). Pullorum disease

with unusual signs in two backyard chicken flocks.J. Avian Dis. 37:895-

897.

Erbeck, D. H.; McLaughlin ,B. G. and Singh, S. N. (1993).Pullorum

disease with unusual signs in two backyardchicken flocks.J. Avian. Dis.

37:895–897.

Eyles, D.; Brown, J.; Mackay-Sim, A.; McGrath, J. and Feron, F. (2003).

Vitamin D3 and brain development. J. Neurosci. 118: 641-653.

Facile, N.; Barbeau, B.; Prevost, M. and Koudjonou, B. (2000). Evaluating

bacterial aerobic spores as a surrogate for Giardia and Cryptosporidium

inactivation by ozone. J. Water Research. 34(12):3238-3246.

Fallacara, D. M.; Monahan, C. M. ; Morishita, T. Y. and Wack, R. F.

(2001). Fecal shedding and antimicrobial susceptibility of selected

bacterial pathogens and a survey of intestinal parasites in free-living

waterfowl.J. Avian Dis. 45:128-135.

Fan, H. H.; Kleven, S. H.; Jackwood, M. W.; Johansson, K. E.; Pettersson,

B. and Levisohn, S.( 1995). Species identification of avian

mycoplasmas by polymerase chain reaction and restriction fragment

length polymorphism analysis.J. Avian Dis. 39:398-407.

Fuhrmann, H. and Sallmann, H. P. ( 2000). Brain, liver and plasma

unsaturated aldehydes in nutritional encephalomalacia of chicks. J. Vet.

Med. 47:149-155.

Garcia, M.; Elfaki, M. G. and Kleven, S. H. (1994). Analysis of the

variability in expression of Mycoplasma gallisepticum surface antigens.J.

Vet. Microbiol. 42:147-158.

Gast, R. K. and Beard, C.W. (1990). Serological detection of experimental

Salmonella enteritidis infections in layer hens.J. Avian Dise. 34: 721-728.

Gast, R. K. and Holt, P. S. ( 1998). Application of flagella-base immunoassays

for serologic detection of Salmonella pullorum.J. Avian Dise. 59: 234-

242.

Gauger, H. C. ( 1934). A chronic carrier of fowl typhoid with testicular

focalization. J. Am. Vet. Med. Assoc. 84:248-251.

Gautier-Bouchardon, A.V.;Reinhardt, A.K.;Kobisch, M. and Kempf, I.

(2002). In vitro development of resistance to enrofloxacin, erythromycin,

tylosin, tiamulin and oxytetracycline in Mycoplasma gallisepticum,

Mycoplasma iowae and Mycoplasma synoviae. J.Vet. Microbiol. 88: 47-

58.

Golden ,M. and Brown , J. (1991). Heterophiles function in healthy chickens

and in chickens with experimentally induced staphylococcal

tenosynovitis.J. Vet. Pathol. 28:419-427.

Gross, W. B. (1990). Factors affecting the development of respiratory disease

complex in chickens.J. Avian Dis. 34: 607–610.

Guesry, P. ( 1998). The role of nutrition in brain development.J. Prev. Med.,

27: 189-194.

Hammodi , A . and Aggad , H. (2008) . Antibioresistance of Escherichia coli

strains isolated from chicken colibacillosis in Western Algeria . J . Turk.

Vet. Anim. Sci. 32(2): 123-126

Heinz, G. H. and Hoffman, D. J. (1996). Comparison of the effects of seleno-

L-methionine, seleno-DL-methionine, and selenized yeast on

reproduction of mallards.J. Environ. Pollution 91:169-175.

Huff, G. R.; Huff, W. E.; Balog, J. M.; and Rath, N. C. (2001). Effect of

early handling of turkey poults on later responses to multiple

dexamethasone-Escherichia coli challenge. Resistance to air sacculitis

and turkey osteomyelitis complex.J. Poult. Sci. 80:1314-1322.

Hulland, T. J. (1993). Muscles and tendons. In: Pathology of Domestic

Animals. Eds, K. V.; Jubb, F.; Kennedy, P. C.; Palmer, N. 4th ed.,

Academic Press California. Pp: 183-264.

Islam, M. N. (2003). Poultry Farms with Subsequent Establishment of

Salmonella Gallinarum \ pullorum Free parent Flocks in Bangaladeh.

M.Sc. Thesis. Agriculture university.

Jacob, J.P.; Gaskin, J. M.; Wilson, H.R. and Ben Mather, F. (2003). Avian

diseases transmissible to humans. J .IFAS .2:1-3.

Jeffery, J. S.; Galey, F. D.; Meteyer, C. V.; Kinde, H. and Rezvani , M.

(1994). Type C botulism in turkeys: Determination of the median toxic

dose. J.Vet. Diagn. Invest. 6:93-95.

Jensen, W. I. and Price, J. I. (1987). The global importance of type C botulism

in wild birds. . In: Avian Botulism: An Intrnational Perspective Eklund,

M. W. and Dowell, V. RCharles C Thomas. (editors): Springfield, IL,

33-54.

Jianhua, H.; Ohtsuka, A. and Hayashi, K. (2000). Selenium influences

growth via thyroid hormone status in broiler chickens. British J. Nutr.

84:727-732.

Jindal, N.; Raja, N.; Kumar, S.; Narang, G. and Mahajan, N. K. (1999).

Salmonella gallinarum and Salmonella enteritidis infections in poultry in

some parts of Haryana. J.Indian. Veterinar. 76: 63-564.

Johnson, R.; Norstrom, E. and Soderstrom, K. (2000). Increased expression

of endogenous biotin, but not BNDF, in telencephalic song regions during

zebra finch vocal learning.J. Dev. Brain Res., 120: 113-123.

Kannan, Y.; Harayama, H. and Kato, S. (1997). Effects of dietary calcium

levels on the histomorphology of proximal tibia in vitamin D-deficient

chicks. Jap.J. Poult. Sc. 34:124-131.

Khan, F. R.; Rahman, M. B.; Khan, M.S.; Nazir, K. H.; and Rahman, M.

M. (2005). Seroprevalence of Salmonella and Mycoplasma gallisepticum

infection and plasmid profile analysis of isolated Salmonella. 11th

BSVGER Annual Scientific Conference, Bangladesh Society for

Veterinary Education and Research, Bangladesh Agricultural University,

Mymensingh-2202, Bangladesh, 29:27.

Kleven, S. H. (1997). Mycoplasma synoviae infection In: Diseases of Poultry.

10th ed. Calnek, B. W. ; Barnes, H. J.; Beard, C. W.; McDougald, L. R.

and Saif, Y. M. (eds). Iowa State University Press, Ames, IA. Pp: 220-

228.

Lee, M. D. and Arp, L. H. (1998). Colibacillosis. In: .). A Laboratory Manual

for the Isolation and Identification of Avian Pathogens.Swayne, D. E.;

Glisson, J. R. ; Jackwood, M. W. ; Pearson, J. E. and Reed, W. M.

(editors) Am. Assoc. Avian Pathologists: Kennett Square. Pp: 14-16.

Lee, C. W.; Brown, C.; and Hilt, D. A. ( 2004). Nephropathogenesis of

chickens experimentally infected with various strains of infectious

bronchitis virus. J. Vet. Med. Sci. 66(7):835-840.

Leitner, G.; Waiman, R. and Heller E. (2001). The effect of apramycin on

colonization of pathogenic Escherichia coli in the intestinal tract of

chicks. J.Vet. Q. 23:62-66.

Ley, D. H., and Yoder, H. W. (1997). Mycoplasma gallisepticum infection In:

Diseases of Poultry. 10th ed. Calnek, B. W. ; Barnes, H. J.; Beard, C. W.;

McDougald, L. R. and Saif, Y. M. (editors). Iowa State University Press,

Ames,U.S. Pp: 194-207.

Lierz, M. (2003). Avian renal disease: pathogenesis, diagnosis, and therapy.

J.Vet. Clin. North. Am. Exotic Am .Pract. 6:29-55.

Lutful Kabir, S. M. (2010). Avian Colibacillosis and Salmonellosis: A Closer

Look at Epidemiology, Pathogenesis, Diagnosis, Control and Public

Health Concerns. J. of Environmental Research and Public Health.

54:72-81.

MacDonald, P.N.; Sherman, D. R.; Dowd, S.C.; Jefcoat, J.r. and DeLisle,

R.K. (1995). The vitamin D receptor interacts with general transcription

factor IIB. J. Biol. Chem., 270: 4748-4752.

Mankin, H.J.(1994). Metabolic bone disorder. J. bone and joint

surgery.76:160-188.

McNamee, P. T. and Smyth, J. A. (2000). Bacterial chondronecrosis with

osteomyelitis (‘femoral head necrosis’) of broiler chickens: A review.J.

Avian Pathol. 29:253-270.

Mitchell, W. R. and Rosendal, S. (1987). Type C botulism: The agent, host

susceptibility, and predisposing factors. In : Avian Botulism: An

International Perspective Eklund, M. W. and Dowell, V. R. Charles C

Thomas(Eds.): Springfield, IL, 57-68.

Morrow, C. J.; Bradbury, J. M.; Gentle, M. J. and Thorp, B. H. (1997).

The development of lameness and bone deformity in the broiler following

experimental infection with Mycoplasma gallisepticum or Mycoplasma

synoviae.J. Avian Pathol. 26:169-187.

Noormohammadi, A. H.; Markham, P. F.; Hithear, K. G. W.; Walker,

I.D.; Gurevich, V.A.; Ley, D.H. and Browning, G.F. (1997).

Mycoplasma synoviae has two distinct phase-variable major membrane

antigens, one of which is a putative hemagglutinin.J. Infect. Immun.

65:2542-2547.

Notermans, S.; Havelaar, A. H. and Schellart, J. (1980). The occurrence of

Clostridium botulinum in raw-water storage areas and their elimination in

water treatment plants. J. Water Research. 14(11): 1631-1635.

Pattison, M.; McMullin, P. ; Bradbury, j.; Alexander, D. (2008). Poultry

disease .6th ed .Toronto. Pp: 43-45.

Pennycott, T. W. and Duncan G. (1999). Salmonella pullorum in the common

pheasant (Phasianus colchicus).J. Vet. Rec. 144:283-287.

Pezzlo, M. (1992). Identification of commonly isolated aerobic gram-positive

bacteria. In: Clinical Microbiology Procedures Handbook. Isenberg, H.D.

(ed)., vol. American Society for Microbiology: Washington, DC, 2001-

2002.

Pomeroy, B. S., and Nagaraja, K. V. (1991). Fowl typhoid. In : Diseases of

Poultry. B. W.; Barnes, H. J.; Beard, C. W. ; Reed, W. M. and Yoder, H.

W. (eds). 9th ed, University Press. Iowa State. Pp: 87–99.

Puls, R. (1994). Mineral Levels in Animal Health: Diagnostic Data. 2nd ed.

Clearbrook, BC, Sherpa International. Pp: 26-296.

Quinn, P. J.; Markey ,M. E, B.; and Carter, G. R. (1994).

Enterobacteriaceae. In: Clinical Veterinary Microbiology. Wolfe

Publishing, London, UK. Pp: 209–236.

Rennie, S.; Whitehead, C. C. and Thorp ,B. H.( 1993). The effect of dietary

1,25-dihydroxycholecalciferol in preventing tibial dyschondroplasia in

broilers fed on diets imbalanced in calcium and phosphorus. Br. J. Nutr.

69:809-816.

Ritchared, K . G. (1997). Salmonella Infection. in Disease of poultry . Calnek,

B . W.; Barens, H . J.; Beared, C. W.; Mcdougald, L. r . and Saif, Y.

M.(editors) . 10th ed. Mosby-Wolfe. UK. Pp471-474

Rober , E. and Porte, J. ( 1998). Bacterial Enteritiedes of poultry. J. Poultry

Science. 77: 1159 -1165.

Rock, T. E.; Smith, S. R. and Nashold, S. W. (1998). Preliminary evaluation

of a simple in vitro test for the diagnosis of type C botulism in wild birds.

J Wildlife Dis. 34:744-751.

Salem, M.; Odor. E. M., and Pope, C. (1992). Pullorum disease in Delaware

roasters. J.Avian Dis 36:1076-1080.

Salisch, H.; Hinz, K. H.; Graack, H. D. and Ryll, M. (1998). A comparison

of a commercial PCR-based test to cultur methods for detection of

Mycoplasma gallisepticum and Mycoplasma synoviae in concurrently

infected chickens. J.Avian Pathol. 27:142-147.

Samad, M. A. (2005). Avian salmonellosis. In: Poultry Science and Medicine.

1st ed. Lyric Eric Prokasoni, Bangladesh Agricultural University

Campus, Mymensingh, Bangladesh, Pp.504-513.

Sandhu, T. S. (1991). Immunogenicity and safety of a live Pasteurella

anatipestifer vaccine in White Pekin ducklings: Laboratory and field

trials. J.Avian Pathol. 20:423-432.

Scherer, C. S. and Baker, D. H. (2000). Excess dietary methionine markedly

increases the vitamin B-6 requirement of young chicks. J. Nutr.

130:3055- 3058.

Seo, E. G.;Einhorn, T.A. and Norman, A. W. (1997). 24R,25-

dihydroxyvitamin D-3: An essential vitamin D-3 metabolite for both

normal bone integrity and healing of tibial fracture in chicks. J.

Endocrinology 138:3864-3872.

Shivaprasad, H. L. (2003). Pullorum disease and fowl typhoid. In: Diseases of

Poultry, Saif, Y.M.; Barnes, H.J.; Glisson, J.R.; Fadly, A.M.,

McDoughald, L.R. and Swayne, D.E. (eds). 10th ed. Iowa State

University Press. Ames, U.S. Pp: 568-579.

Smart, J. L.; Roberts, T. A. and Underwood, L. ( 1987). Avian botulism in

the British Isles. In: Avian Botulism: An International Perspective

Eklund, M. W. and Dowell, V. R. Charles C Thomas (ed).Springfield,

IL, 111-122.

Smith, L. D.; Charles, C.; Thomas: (1975). The Pathogenic Anaerobic

Bacteria, 2nd ed. Springfield, IL, 203-229.

Snoeyenbos, G. H. (1991). Pullorum disease. In: Diseases of Poultry. 9th ed.

Calnek, B. W. ; Barnes, H. J. ; Beard, C. W. ; Reid, W. M. and Yoder,

H. W. (eds). University Press. Iowa State. Pp: 73-86.

Styles, D. K., and Phalen, D.N. (1998). Clinical avian urology. Seminars in

Avian and Exotic Pet Medicine: 7(2):104–113.

Tiong, S. K. (1990). Mycoplasmas and acholeplasmas isolated from ducks and

their possible association with pasteurellas. Vet. Rec. 127:64-66.

Varalakshmi, P.; Shamila, Y. and Latha, E. (1990). Effect of Crataeva

nurvala in experimental urolithiasis. Journal of Ethnopharmacology 28:

313-321.

Warrell, D. A.; Cox, T. M.; Firth, J. D. and Benz, E. J. (2003). Oxford

Textbook of Medicine. 4th ed. Oxford: Oxford University Press. Pp: 382-

383.

Whitehead, C. C. (1998). A review of nutritional and metabolic factors

involved in dyschondroplasia in poultry. J. App. An. Res. 13:1-16.

Wilcox, C. S.; Patterson, J. and Cheng , H. W. (2009) . Research notes use

of thermography to screen for subclinical bumble foot in poultry. J.

Poultry Scie. 88:1176-1180.

Wong, E., Mikaelian, I., Desnoyers, M. & Fitzgerald, G.(1999) Pansteatitis

in a free-ranging red-tailed hawk (Buteo jamaicensis). Journal of Zoo and

Wildlife Medicine, 30(4), 584–586.