COMMERCIAL BROILERS
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SIMILAR BASIC REQUIREMENTS
…FOR…
BROODING
NUTRITION
HOUSING AND EQUIPMENT
MANAGEMENT
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Brooding
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ALL THE BIRD’S BODY
SYSTEMS ARE DEVELOPING
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1-DAY OLD BROILER CHICK
RESIDUAL YOLK
IMMATURE
DIGESTIVE TRACT
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Gut development
HATCH
1 WEEK
OF AGE
TOTAL MASS IS 4 FOLD
GREATER THAN REST OF BODY
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DURING EMBRYOGENESIS
THE DIGESTIVE TRACT DEVELOPS
BEFORE THE BRAIN
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BROODING
COMMERCIAL SCALE
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BROODING
SMALL SCALE
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BROODING UNITS
LAMP-TYPE BROODER
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BROODING
BROODING HEAT SOURCES
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BROODING UNITS
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WHAT IS THE BEST WAY TO DETERMINE
IF THE CHICKS ARE COMFORTABLE
IN THE BROODER ?
THE CHICKS WILL TELL YOU
IF THEY ARE COMFORTABLE
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BROODING
THE CHICKS WILL TELL YOU IF THEY ARE COMFORTABLE
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BODY WEIGHT
TODAY’S MEAT-TYPE BIRDS
GROW VERY RAPIDLY
1000 HOURS
AGE
MOST CRITICAL PERIOD
42 DAYS
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Gut development
….FACT….
WHEN FEED INTAKE DECLINES
GUT DEVELOPMENT DECLINES
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Crop fill
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IMPORTANT NUTRITIONAL CONCEPT
NUTRITION
IS FIXED
NUTRITION
IS NOT FIXED
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NUTRITIONALLY SPEAKING
WHAT ARE THE ONLY SIX
THINGS CHICKENS NEED ?
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SIX MAJOR NUTRIENTS
CARBOHYDRATE
LIPID
PROTEIN
VITAMINS
MINERALS
WATER
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VERY IMPORTANT CONCEPT OF
NUTRITION TO REMEMBER
NOT
…..ENERGY IS
A NUTRIENT…..
IT IS A “PROPERTY” OF THREE NUTRIENTS
CARBOHYDRATE
LIPID
PROTEIN
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VERY IMPORTANT CONCEPT OF POULTRY
NUTRITION TO REMEMBER
MOST POULTRY
EAT THE AMOUNT OF FEED THEY NEED IN
ORDER TO MEET AN ENERGY REQUIREMENT
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IMPORTANT FACT TO REMEMBER
…TODAY…
FEED COSTS REPRESENT APPROXIMATELY
75% OF THE TOTAL COST OF
PRODUCING MEAT AND EGGS
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“General Nutrition”
“CONVENTIONAL PRODUCTION”
1) USE THE CORRECT FEED FOR EACH AGE & BIRD TYPE
STARTER
GROWER
FINISHER
LAYER
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GIZZARD & PROVENTRICULUS
(VENTRICULUS)
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KOILIN LINING
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KOILIN LINING OF GIZZARD
GROOVES
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GRIT
FED FOR ONLY ONE PURPOSE
NOT NECESSARY IF MASH OR PELLETS ARE FED ALONE
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GIZZARD
GRIT
KOILIN LAYER
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HOW MUCH WATER WILL POULTRY DRINK
?
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BROILER AGE AND WATER CONSUMPTION
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DAILY WATER CONSUMPTION
“BROILERS”
(UNDER NORMAL CONDITIONS)
DAYS OF AGE X 6 ML
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Diseases of Poultry
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Newcastle diseases Virus
(ND/Ranikhet )
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Newcastle disease virus (NDV)
• A type strain for avian paramyxoviruses. Members of this
family have a single stranded, linear, RNA, with an elliptical
symmetry. The total genome is roughly 16,000 nucleotides.
Replication of the virus takes place in the cytoplasm of the
host cell.
• This family also includes important viruses such as mumps,
human parainfluenza, sendai, simian virus-5 and recently
emerged nipah and hendra viruses.
• NDV particle
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Newcastle Disease (ND)
•
•
•
•
•
ND is caused by Newcastle disease virus
A disease with high infectivity.
Mortality rate is extremely high in chicken.
Depending on the virus strain responsible.
Practically, all avian species can be affected.
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Clinical symptoms of ND
Sudden death with few clinical signs
• Respiratory symptoms
• Nervous signs
• Loss of appetite, depression, and lethargy
• Dark greenish diarrhea
• Decreased egg production
There is a marked
hemorrhage of the
comb, wattle, and
adjacent skin.
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Newcastle disease
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Newcastle disease
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Newcastle disease
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Newcastle disease
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Newcastle disease
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Newcastle disease
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Newcastle disease
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Zoonotic importance
 Newcastle disease Newcastle Disease Virus (NDV) is highly
contagious.
 Transmission occurs by exposure to faecal and other excretions
from infected birds, and through contact with contaminated
feed, water, equipment and clothing.
 Exposure of humans to infected birds can cause mild influenzalike symptoms and conjunctivitis, an abnormal eye discharge
due to inflammation of the membrane lining the inside of the
eyelid.
 The infection can also cause nasal discharge, sneezing, and
pneumonia. Left untreated, the infection tends to become
chronic, lasting weeks or months.
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Newcastle disease virus (NDV)
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Newcastle disease virus (NDV)
• NDV strains can be classfied into 3 pathotypes
Velogenic strains
Mesogenic strains
Lentogenic strains (vaccine)
• Wild or free-living birds (waterfowls) play a role in the spread
of NDV
• Several outbreaks in many countries
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Transmission of NDV from wild birds
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The NDV genome
• NDV has a single stranded negative-sense RNA genome,
which is approximately15 kb long.
• The genomic RNA contains six genes encoding at least eight
proteins.
• The nucleoprotein(NP), the phosphoprotein (P), and the
large polymerase protein (L) form the nucleocapsid. The
haemagglutinin neuraminidase (HN) and fusion protein (F)
anchored in the lipid bilayer of membrane in the external
envelope,while inner layer of the virion envelope is formed
by the matrix protein (M).
• The two additional non structural proteins, V and W are
formed by the RNA editing process during P gene
transcription.
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Newcastle disease virus (NDV)
8 genotypes of NDV strains can be isolated from the field
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Diagnosis
• Viurs isolation using embryonated eggs or tissue cultures
(chicken kidney cells)
• HA test and HI test using the NDV-specific antiserum
• Pathogenicity test
10-day-old embryo
1-day-old chick
or nucleotide sequencing of the F gene
• Detection of the NDV genome
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Detection methods of the NDV genome
• RT-PCR, RT-nested PCR
(conventional, NP, F, HA, M)
• Real-time PCR
(F, differentiation of genotypes)
• Multiplex PCR
• (NP, F, differentiation of genotypes)
• LAMP
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NDV & Cancer
• NDV selectively replicates in tumour cells and induces death while sparing
normal cells.
• Due to this property, NDV has been exploited as a potential anti-cancer agent in
humans.
• Based on the mechanism by which oncolysis is achieved, NDV has been
classified as lytic or non lytic strains for mammalian cells.
• Lytic strains cause lysis of target cells by inducing changes in the plasma
membrane including syncytia formation.
• These include 73-T31, MTH-68/H32, PV 70133, etc.
• Non lytic strains cause tumour regression slowly by disrupting normal host
cell metabolism.
• This includes most commonly investigated Ulster strain.
• Both strains replicate efficiently in tumour cells and have been investigated as
anti-cancer agents.
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Mechanisms of NDV-induced oncolysis
• First, lytic strains of the virus may simply kill the tumour cells
directly and were found effective in preventing tumours from
further spread.
• Secondly, for non lytic strains, the viral proteins inserted on to
tumour cell membrane after infection may enhance an immune
response.
• Finally, the virus itself may stimulate the host to produce
effector cytokines such as interferons (IFN-γ) or TNF which
activate (NK) cells, macrophages and sensitized T-cells.
• NDV also augments the expression of induced nitric oxide
synthase (iNOS) in infected cells.
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Mechanisms of NDV-induced oncolysis
• There are reports that NDV induces NFκB and up regulates the
expression of MHC I genes.
• NDV induces caspase dependent apoptosis in cancerous cells
by both extrinsic and intrinsic apoptotic pathways.
• It was also found that NDV induces apoptosis by up regulating
the expression of pro-apoptotic p53 and Bax and down
regulating the anti-apoptotic Bcl-2 gene expression in target
cells.
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Broad spectrum antitumour activity of NDV
• Tumours of epithelial origin
(carcinomas including breast, lung, prostate
and colon).
• Neuroectodermal
(melanomas, glioblastmas & neuroblastomas)
• Mesenchymal origin
(sarcomas).
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ClinicalTrials.gov
A service of U.S National institutes of health
Newcastle Disease Virus (NDV) for Cancer Patients Resistant
to Conventional Anti-Cancer Modalities
This study is currently recruiting participants. Verified by
Hadassah Medical Organization, February 2006
Condition
Intervention
Phase
Metastatic Cancer
Procedure: Newcastle Virus
Phase II
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ClinicalTrials.gov
A service of U.S National institutes of health
New Castle Disease Virus (NDV) in Glioblastoma Multiforme
(GBM), Sarcoma and Neuroblastoma
This study is not yet open for participants recruitment. Verified
by Hadassah Medical Organization, August 2010
Condition
Intervention
Phase
Glioblastoma
Sarcoma
Neuroblastoma
Biological:
New Castle Disease Virus
Phase I
Phase II
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Phase I/II Trial of Intravenous NDV-HUJ Oncolytic Virus in
Recurrent Glioblastoma Multiforme
Radiology, and Gaffin Center for Neuro-Oncology, Hadassah University Hospital, Jerusalem 91120, Israel (2009)
Complete tumor response. (A) Patient 09 at baseline, (B) stable disease at
first follow-up, (C) partial response (PR) at second follow-up, (D) PR at 20
weeks from start of virotherapy, and (E and F) complete response at 25 and
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30 weeks from start of virotherapy.
Infectious bursal disease (IBD)
GUMBORO
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Infectious bursal disease (IBD)
• is a highly contagious disease of young chickens caused by
infectious bursal disease virus (IBDV)
• characterized by immunosuppression and mortality generally
at 3 to 6 weeks of age.
• IBDV is a double stranded RNA virus that has a bi-segmented
genome and belongs to the genus Avibirnavirus of family
Birnaviridae.
• There are two distinct serotypes of the virus, but only serotype
1 viruses cause disease in poultry.
• IBDV genome consists of two segments, A and B, which are
enclosed within a nonenveloped icosahedral capsid.
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Infectious bursal disease (IBD)
• The genome segment B (2.9 kb) encodes VP1, the putative
viral RNA polymerase.
• The larger segment A (3.2 kb) encodes viral proteins VP2,
VP3, VP4, and VP5.
• VP2 protein contains important neutralizing antigenic sites and
elicits protective immune response and most of the amino acid
(AA) changes between antigenically different IBDVs are
clustered in the hypervariable region of VP2.
• The virus is attracted to lymphoid cells and especially those of
B-lymphocyte origins.
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Infectious bursal disease (IBD)
• Young birds at around two to eight weeks of age that have
highly active bursa of Fabricius are more susceptible to
disease.
• Birds over eight weeks are resistant to challenge and will not
show clinical signs unless infected by highly virulent strains.
• After ingestion, the virus destroys the lymphoid follicles in the
bursa of Fabricius as well as the circulating B-cells in the
secondary lyphoid tissues such as GALT (gut-associated
lymphoid tissue), CALT (conjuntiva), BALT (Bronchial)
caecal tonsils, Harderian gland.
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Infectious bursal disease (IBD)
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Infectious bursal disease (IBD)
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Infectious bursal disease (IBD)
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FOWL POX
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FOWL POX
• Fowlpox is a worldwide disease of poultry caused by viruses
of the family Poxviridae and the genus Avipoxvirus.
• There are two forms of the disease.
• The first is spread by biting insects (especially mosquitoes)
and wound contamination and causes lesions on the comb,
wattles, and beak. Birds affected by this form usually recover
within a few weeks.
• The second form is spread by inhalation of the virus and
causes a diphtheritic membrane to form in the mouth, pharynx,
larynx, and sometimes the trachea. The prognosis for this form
is poor.
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FOWL POX
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FOWL POX
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FOWL POX
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Infectious laryngotracheitis
(ILT)
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Infectious laryngotracheitis
 Infectious Laryngotracheitis virus is a herpes virus that
causes respiratory disease in chickens.
 characterized by severe dyspnea, coughing, and rales.
 It can also be a subacute disease with lacrimation, tracheitis,
conjunctivitis, and mild rales.
 The acute disease is characterized by the clinical signs and
by finding blood, mucus, and yellow caseous exudate or a
hollow caseous cast in the trachea.
 After recovery, some birds remain carriers for extended
periods and become a source of infection for susceptible
birds. The latent virus can be reactivated under stressful
conditions.
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Infectious laryngotracheitis
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Infectious laryngotracheitis
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Infectious bronchitis
IB
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Infectious bronchitis
• Infectious bronchitis is an acute, rapidly spreading, viral
disease of chickens.
• characterized by respiratory signs, decreased egg production,
and poor egg quality.
• Some strains of the causative virus, infectious bronchitis virus
(IBV), are nephropathogenic. The latter strains produce
interstitial nephritis resulting in significant mortality.
• IBV, a coronavirus, is worldwide in distribution and has
numerous serotypes.
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Infectious bronchitis
• IBV is shed by infected chickens in respiratory discharges and
feces.
• The highly contagious virus is spread by airborne droplets,
ingestion of contaminated feed and water, and contaminated
equipment and clothing of caretakers.
• Naturally infected chickens and those vaccinated with live
IBV may intermittently shed virus for many weeks or even
months.
• Virus infection in layers and breeders occurs cyclically as
immunity declines or on exposure to different serotypes.
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Infectious bronchitis
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Infectious bronchitis
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Infectious bronchitis
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Infectious bronchitis
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Infectious bronchitis
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Stunting syndrome
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Stunting syndrome
• Broiler chicks diseases
• Unknown etiology
• Impaired growth
• Bad feathering
• Bone abnormalities, Maldigestion and malabsorption
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Stunting syndrome
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Stunting syndrome
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Hydropericardium syndrom
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Hydropericardium syndrom
• Avian adenoviruses (AAV) in chickens are the etiologic agents
of 2 important diseases known as inclusion body hepatitis
(IBH) and hydropericardium syndrome (HP).
• Characterized by the hepatitis, pale kidneys and pulmonary
edema.
• Mortality varies from 12-75%
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Hydropericardium syndrom
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Hydropericardium syndrom
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Hydropericardium syndrom
Hydropericardium syndrom
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Marek’s Disease
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Marek’s Disease
• Marek's disease is a highly contagious viral neoplastic
disease in chickens. It is named after József Marek.
• An infectious and highly contagious diseases caused by
herpesvirus.
• Characterized by proliferation of lymphoid cells and their
aggregation in any part of body but mostely peripheral nerve.
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Marek’s Disease
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Marek’s Disease
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Marek’s Disease
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Marek’s Disease
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Marek’s Disease
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Marek’s Disease
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