محاضرة اليوم الثالث د احمد البستاوي

AVIAN VIRAL AND BACTERIAL
RESPIRATORY DISEASES
Presented By
Dr. Ahmed Ragab El-Bestawy
BVs, MVs & Ph.D.
Lecturer of Poultry Diseases
Fac. Vet. Med., Damnhour
Univ.

Diseases causing Resp signs:
o Viral:
AI, ND, IB,ILT, TRT, Adeno, Reo, Pox wet form and
MD ( non specific)
o Bacterial:
IC, MG, Ecoli, FC, ORT and Chlamydia.
o Fungal: Asperigellosis.
o Parasitic: Syngamus trachea, Cryptosporidium
o Nutritional: Vit A ↓.
o Miscellaneous: Chilling and Ammonia

‫إصاتح‬E.coli ‫ثاَىَح‬ ‫كإصاتح‬

Influenza Virus
 Family Orthomyxoviridae
 Three main types
 Type A
 Multiple species
 Type B
 Humans
 Type C
 Humans and swine

Influenza A
 Multiple species
 Humans
 Avian Influenza
 Most virulent group
 Classification by surface antigens
into subtypes
 Hemagglutinin (H or HA)
 Neuraminidase (N or NA)

Surface Antigens
and Subtypes
 18 HA and 11 NA for influenza A
 Hemagglutinin (HA)
 Function: Sites for attachment to infect host cells
 Neuraminidase (NA)
 Function: Remove neuraminic acid from mucin and
release from cell

Avian Influenza
 Pathogenicity based on genetic features and/or
severity of disease
in poultry
 Low pathogenic AI (LPAI)
 H1 to H18 subtypes
 Highly pathogenic AI (HPAI)
 Some H5 or H7 subtypes
 LPAI H5 or H7 subtypes can mutate
into HPAI

H9 subtype viruses generally exist as low pathogenicity influenza
viruses causing mild to moderate disease. However, they have been
associated with severe morbidity and mortality in poultry as a result
of co-infection with other pathogens.
The first H9N2 influenza virus was isolated from turkeys in Wisconsin
in 1966.
H9N2 subtype influenza viruses were isolated from pigs in Hong Kong
in 1998 and subsequently from two sick children in 1999; six
additional human infections were reported from China

Recent studies have shown that H9N2 viruses may have contributed to
the genetic and geographic diversity of H5N1 viruses.
During the last two decades, antigenic and genetic analysis of H9N2
isolates showed their gradual and complex evolution revealing
extensive re-assortments to generate multiple novel genotypes (7)
with gene segments from different lineages.

Transmission pathways:
 Low biosecurity is a high risk.
 Market systems
 Mainly Air born

Pathogenicity:
Severe morbidity and mortality in poultry results
from:
1. co-infection with other pathogens.
2. Live Vaccines (ND &/or IBV)
3. Management factor.

Organ affinity:
 Respiratory
 Renal
 Reproductive
 Nervous

Clinical signs and PM lesions
 Broilers:
Swelling of head.
Respiratory sound.
Decreased feed in take.
Intestinal ballooning.
Pancreatitis
Nephritis

 Layers and Breeders:
Depression and slight to moderate decrease
of egg production.
Intestinal twisting and egg peritonitis
Pancreatitis (Thickening of pancrease)
Nephritis

•‫انتش‬ ‫انصفح‬‫شَحُح‬:
‫انطُىس‬ ‫اَفهىَضا‬ ‫يشض‬ ٍ‫ف‬ ‫انتششَحُح‬ ‫انصفاخ‬ ‫أهى‬ ٍ‫ي‬(‫عاو‬ ‫تشكم‬)ٍ‫ه‬:
.1‫وخىد‬ٌ‫احتما‬ٍ‫ف‬ ‫كًا‬ ‫انمصثاخ‬ ٍ‫ف‬‫انُُىكاسم‬،
.2ً‫عه‬ ‫أَضفح‬‫انًعذج‬‫انغذَح‬‫األيعاء‬ ،
.3‫سئىي‬ ‫انتهاب‬
.4‫تانثُكشَاط‬ ‫انتهاب‬
.5‫تانًثُط‬ ٌ‫احتما‬
.6‫وانمهة‬ ٍ‫انثط‬ ٌ‫دهى‬ ً‫عه‬ ‫أَضفح‬
.7‫انذ‬ ٍ‫ف‬‫خاج‬، ‫داكُح‬ ‫تُكضَح‬ ٍ‫أياك‬ ‫وخىد‬ ‫يع‬ ‫انثُط‬ ٍ‫ف‬ ‫َضف‬ ‫َالحظ‬ ‫انثُاض‬
.8‫انًثُط‬ ‫اَفداس‬ ‫َتُدح‬ ‫تانسىائم‬ ‫يًهىء‬ ٌ‫َكى‬ ٍَ‫انثشَتى‬ ‫انتدىَف‬ ‫كزنك‬.
.9‫اندفاف‬ ‫عالياخ‬ ‫سىي‬ ‫َالحظ‬ ‫ال‬ ‫لذ‬ ‫انالحى‬ ‫انذخاج‬ ٍ‫ف‬‫أخشي‬ ‫تششَحُح‬ ‫صفح‬ ٌ‫أ‬ ٌ‫تذو‬ ‫انًصاتح‬ ‫اإلفشاخ‬ ً‫عه‬.

H9N2 vaccines
 Inactivated vaccines
 Must be Autogenous
 Country/regional variation
 Vaccine use will:
Prevent clinical signs
Reduce virus shedding

Dose of the vaccine 0.5 ml .
Administration S/C lower back of the neck .
Age of vaccination:
Broiler one Dose at 7-10 day old .
Breeder & layer 1st Dose 10 D.O
2 nd Dose 40 D.O
3 rd Dose 16-18wk .

Currently available H5 vaccine
A. Inactivated homologous vaccine :
B. Inactivated heterologous vaccines:
The vaccine have the same H type as the field but
heterologous neuraminidase.
Clinical protection and reduction in viral shedding are ensured
by the immune reaction caused by H and N used as marker of
field infection.

Marek‘s with H5
Fowl Pox with H5
Other vectors as ILT or lasota with H5

 Mycoplasmas are bacteria that lack cell wall and
belong to the class Mollicutes.
‫ّهزكجبد‬ ‫الجٌظليي‬ ‫هثل‬ ‫األدّيخ‬ ‫لجؼط‬ ‫هقبّهخ‬ ‫الويكْثالسهب‬ ‫إى‬
‫الظلفب‬.

Species usual host
A.Laidlawii Various
M.Anatis Duck
M.Anseris Goose
M.Butenois Buteo Hawk
M.Cloacale Turkey,goose
M.Columbinasale Pigeon
M.Columbinum Pigeon
M.Columborale Pigeon
M.Corogypsi Black Vulture
M.Falconis Saker Falcon
M.Gallinarum Chicken
M.Gallinaceum Chicken
M.Gallisepticum Chicken,turkey,house
finish.
M.Gallopavonis Turkey
M.Glycophilum Chicken
M.Gypis Griffon Vulture
M.Imitis Duck,goose,partridge
M.Iners Chicken
M.Iowae Turkey

 Species usual host
 M.Glycophilum Chicken
 M.Gypis Griffon Vulture
 M.Imitis Duck,goose,partridge
 M.Iners Chicken
 M.Lipofaciens Chicken
 M.Meleagridis Turkey
 M.Pullorum Chicken
 M.Sturni European starling
 M.Synoviae Chicken,turkey
 M.Gallorale Chicken

Major mycoplasma species in poultry
1.M. gallisepticum:
Chronic respiratory disease(CRD in chickens
and infectious sinusitis in turkeys)
embryo mortality, lameness, eye lesions.
2. M. Synoviae:
Infectious tenosynovitis in chickens
Respiratory disease(Turkeys), embryo mortality.
3. M. Meleagridis:
Respiratroy disease, leg weakness, embryo
mortality in turkeys.
4. M. iowae: embryo mortality, leg abnormalities in turkeys.

MYCOPLASMA GALLISEPTICUM INFECTION
 Commonly known as chronic respiratory disease (CRD) of
chickens and infection sinusitis in turkeys.
 Characterized by respiratory rales, coughing, nasal
discharge, ,conjunctivitis ,growth retardation and drop in
egg production in layers.

ECONOMIC SIGNIFICANCE
1. Increased condemnations (air saculitis) (5-10%)
2. Increased downgrading of carcasses (10-25%)
3. Reduced feed efficiency(5-15%)
4. Reduced egg production (10-20%)& efficiency
5. Increased embryo mortalities (5-20%)
6. Increased mortality rate (5-30%)
7. Increased medication costs
8. Increased costs of prevention and control ,include
surveillance (serology,culture,isolation, and
identification)

‫انعايم‬‫الوظجت‬Cause
ُْ‫كبئي‬‫دقيق‬‫يحتل‬‫هزحلخ‬‫هتْططخ‬‫ثيي‬‫الجزاثين‬‫ّالفيزّطبد‬ٔ‫ّيظو‬
‫هبيكْثالسهب‬‫غبليظيجتكن‬Mycoplama Gallispticum‫حيث‬َ‫ل‬
‫ثؼط‬‫صفبد‬‫الجزاثين‬‫ّالفيزّطبد‬‫ّيختلف‬‫ػي‬ٔ‫األّل‬‫ّالثبًيخ‬
‫ثجؼط‬‫الصفبد‬‫أى‬ٍ‫ُذ‬‫الكبئٌبد‬‫صغيزح‬ً‫ا‬‫جذ‬‫ليض‬‫لخليتِب‬‫غشبء‬.
‫تتلْى‬ً‫ب‬‫طلجي‬‫ثصجغخ‬‫غزام‬.
‫تتؼبيش‬‫الويكْثالسهب‬‫طجيؼيب‬ٔ‫ف‬‫صْرح‬‫غيز‬‫هوزظخ‬ٔ‫ف‬‫الجِبس‬
ٔ‫التٌفظ‬ْٓ‫الؼل‬‫للطبئز‬.

Transmission- MG/MS
Vertical (transovarian)
MG/MS are transmitted in eggs laid by infected
breeders
 Peak transmission is minimal < 3% of eggs

Horizontal Transmission:
Dust, equipments, wild birds as sparrows,
trucks, feed, workers, vet. doctors, insects
as cats, dogs, contaminated vaccines.

Infected chickens transmit MG/MS
through aerosols (short distances)
contaminated feed and water
MS spreads more rapidly than MG

FEED
Skin: <4 hrs
Ear: 4 hrs
Nose: 1 day
Hair: 3 days
Feathers: 4
days
Feed: 4 hrsRubber: 2
days
Shavings: 8
hrs
Wood: 1 day
Cotton: 4
days
Mechanical transmission and survival of
MG

‫الويكْثالسهب‬ ‫لوزض‬ ‫الوِيئخ‬ ‫الؼْاهل‬

‫المعقد‬ ‫المسمن‬ ‫التنفسى‬ ‫المرض‬
CCRD
‫االجهاد‬ ‫عوامل‬
Stress
‫الثانوية‬ ‫البكتيريا‬
E coli‫الميكوبالزما‬

Stress
‫االخهاد‬ ‫عىايم‬
 Bad ventillation ‫التِْيخ‬ ‫طْء‬
 Cold ‫الجزّدح‬
(Temp. Variation)
 High amonia ‫األهًْيب‬
 Dust ‫األتزثخ‬
 Mycotoxins ‫الفطزيخ‬ ‫الظوْم‬
 Immunosuppression
ٔ‫الوٌبػ‬ ‫التثجيط‬
 Poor feed ‫الؼلف‬ ‫طحت‬ ‫قلخ‬
 Overcrowding ‫التشاحن‬

MG is an intracellular
microorganisms

 The latent status, i.e., when the mycoplasma is not
recognized by the host immune system, may be
explained by its intracellular location due to
environmental pressure, as can be exemplified by the
presence of antimicrobials in host tissues for the
treatment of MG, MS or MM infection of birds.

 The frequent changes on surface antigens (antigenic
variations due to defective DNA repair system) allow
mycoplasmas to evade the host immune system, and
facilitate their survival when adhered to the host
respiratory tract

Their pathogenic
mechanism for disease include adherence to host target
cells

Destruction of cilia on endothelial
cells

Mycoplasma gallisepticum Invades Chicken
Erythrocytes during Infection

INCUBATION PERIOD
Varies from 6-21 days
Varies depend on :
 MG strain virulence
 Complicating infection
 Environmental and other stressors
‫ّالزّهي‬ ‫الذجبج‬ ‫قطؼبى‬ ٔ‫ػل‬ ‫األػزاض‬ ‫تظِز‬ ‫هب‬ ً‫ب‬‫غبلج‬
‫الجيط‬ ‫إًتبج‬ ‫ثذء‬ ‫ػٌذ‬

1.Coughing
2.Sneezing
3.Gasping
4.Rales
5.Ocular and nasal discharge
6.Decrease in feed consumption
7.Pale comb and head
8.Increased mortalities
Broilers

Mycoplasmosis in Breeders
 Reduce egg production (MG free hens laid 15 more eggs
per hen housed than unvaccinated MG infected birds over a
45 week laying period)
 lower fertility (MG & MS)
 lower egg shell quality
 Pipped embryo
 poor chick quality
 smaller chicks
 greater cost per chick

PM lesions
Catarrhal inflammation of sinuses,
trachea, and bronchi.
Air-sacculitis:

‫انًاَكىتالصيا‬ ‫إصاتح‬ ‫دسخاخ‬:
•‫درجخ‬‫صفش‬‫شفبفخ‬ ّ ‫ًظيفخ‬ ‫الِْائيخ‬ ‫االكيبص‬.
•‫درجخ‬1‫الِْائيخ‬ ‫االكيبص‬ ‫في‬ ‫ػتبهخ‬.
•‫درجخ‬2‫الِْائيخ‬ ‫االكيبص‬ ‫في‬ ‫تعخن‬.
•‫درجخ‬3‫التِبثي‬ ‫ًعح‬ ‫ّجْد‬ ‫هغ‬ ‫لحوي‬ ‫هٌظز‬
‫الِْائيخ‬ ‫االكيبص‬ ‫هي‬ ‫ّاحذح‬ ‫جِخ‬ ‫في‬.
•‫درجخ‬4‫التِبثي‬ ‫ًعح‬ ‫ّجْد‬ ‫هغ‬ ‫لحوي‬ ‫هٌظز‬
‫في‬‫الِْائيخ‬ ‫االكيبص‬ ‫هي‬ ‫جِتيي‬.

‫صفش‬ ‫دسخح‬:‫َظُفح‬ ‫و‬ ‫شفافح‬ ‫انهىائُح‬ ‫االكُاط‬

Mycoplasma Score 1. No pericarditis and perihepatitis

‫الهىائية‬ ‫االكياس‬ ‫في‬ ‫تضخم‬
‫االكياس‬ ‫في‬ ‫نضح‬ ‫يىجذ‬ ‫ال‬
‫االصابة‬ ‫درجة‬2Dr Lloyd Reeve-Johnson, PhD Thesis, Veterinary Epidemiology
and Economics Research Unit, University of Reading

‫مع‬ ‫الهىائية‬ ‫االكياس‬ ‫في‬ ‫تضخم‬
‫إلتهابية‬ ‫إفرازات‬ ‫و‬ ‫نضح‬ ‫وجىد‬
‫الكبذ‬ ‫و‬ ‫القلب‬ ‫على‬ ‫إصابة‬ ‫ال‬
Dr Lloyd Reeve-Johnson, PhD Thesis, Veterinary Epidemiolo
and Economics Research Unit, University of Reading
‫درجة‬3:‫الهىائية‬ ‫لالكياس‬ ‫شاملة‬ ‫إصابة‬

ٍ‫ساَُىف‬ ‫ياَكىتالصيا‬
Infectious Synovitis
‫االستطح‬ ‫و‬ ‫انًفاصم‬ ٍ‫ف‬ ‫انتهاب‬
‫تُفسُح‬ ‫إصاتاخ‬

Options to assist in eradication
effort or to reduce losses
Medication
Vaccination

Medication
1. Treat MG respiratory diseases
2. Reduce egg production losses
3. Reduce MG shedding and transmission.
4. Reduce severity of lesions and clinical
signs.
5. Significantly reduce population of MG in
the respiratory tract.
Antimycoplasmal drugs have been used
to :

Treatment
.1ٍُ‫تهًُكىس‬
.2ٍُ‫تُايىن‬
.3ً‫دوك‬‫س‬ٍُُ‫كه‬-ٍُ‫تتشاسُكه‬ ً‫أوكس‬
.4ٍُ‫َىسفهىكساس‬-ٍُ‫سُثشوفهىكساس‬-ٍُ‫اَشوفهىكساس‬
.5ٍُ‫سثُشاياَس‬
.6ٍُ‫نُُكىياَس‬
.7ٍَ‫تاَهىص‬
.8ٍُ‫اسَثشويُس‬
‫انمىنىَُح‬ ‫تانعصُاخ‬ ‫انثاَىَح‬ ‫األصاتح‬ ‫حانح‬ ً‫ف‬CCRD‫عًم‬ ‫َتى‬
‫انحُىي‬ ‫انًعاد‬ ‫استخذاو‬ ‫َتى‬ ‫عهُه‬ ‫وتُاءا‬ ‫حساسُح‬ ‫اختثاس‬.

Antimycoplasmal Drugs
MIC (μg/ml)Antimicrobial
0.048Tilmicosoin
0.006-0.39Tiamulin
0.04Doxycycline
0.05Enrofloxacin
0.06Ciprofloxacin
0.08Lincomycin
0.4-4Tylosin
0.08Erythromycin

ANTIMYCOPLASMA PLANNING
BROILER
Dose Days
I 1,2,3
II 20,21,22 (With live vaccines
(ND)

Antimycoplasma Planning
Layer-Breeder
Dose Days
I 1,2,3
II For 3 days (20,21,22)
III For 3 days during the 9th week
IV For 3 days during the 17th week
V Feed additive ( premix ) continously
during laying

MG and MS Vaccination
Vaccine types:
MG
􀂾 F-strain MG
􀂾 Strain 6/85
􀂾 TS-11
􀂾 Bacterin – inactivated
MS
􀂾 MS-H
􀂾 MG Bacterin- inactivated

Newcastle Disease
Synonyms
Pseudo fowl plaque
Avian distemper
Pests
Avian pneumoencephilitis

Definition
It’s usually an acute highly contagious
septicemic disease of domestic and wild
birds characterized by respiratory
symptoms accompanied or followed by
nervous manifestation with high losses in
susceptible birds.
(Disease common & serious in Egypt)

Strains of the virus vary in
virulence (Pathogenecity):
a) Velogenic strains: Texas, Herts, highly virulence
used for challenge. Embryo receiving minimal lethal
dose die ( 50hrs ).
b) Mesogenic strains: Komarov, used as a vaccine.
Moderate in pathogencity for CE (2-3 day) for ODO
& 8-10 wks (death rarely).
c) Lentogenic strains: F1, B1, lasota , low virulence
used as a vaccine. Pathogenicity for CE die after
100 hrs. For ODO, 8-10 wks old in apparent disease.
d) Apathogenic: Enteric strains

Avian Paramyxovirus – 1 (APMV-1)
Order: Mononegavirales
Family: Paramyxoviridae
Sub-Family: Paramyxovirinae
Genera: Avulavirus
Serogroups: 9 Serogroups (APMV 1 – 9)
(PPMV-1): Pigeons & Doves - Antigenic variant of NDV
HN
L, NP, P (V)
Newcastle Disease Virus

NP: Nucleoprotein
P: Phosphorilated protein (Overlapping V gene protein)
M: Matrix
F: Fusion with host cell membrane (Smaller spike)
HN: Hemagglutinin / Neuraminidase activities (Largest spike)
L gene: RNA-Directed RNA polimerase (Nucleocapside)
NP P M F0 HN L
Genomic Features
Enveloped pleomorphic RNA virus
100-500 nm size
Single-stranded; Non-segmented
Negative sense (15kb)
Helical nucleocapside symmetry
(Herring-bone like structure)
NDV
Genome
Features
Lentogenic
112RRQRRF117
Velogenic

Although all NDV isolates characterized to date belong to a single
serotype, the avian paramyxovirus serotype 1 (APMV-1), significant
genetic diversity has been recognized among different NDV isolates.
Historically, NDV isolates have been classified into two major groups
(class I and II), based on their genome lengths and the nucleotide
sequences of their genomes.
Class I viruses are distributed worldwide and have been isolated
mainly from waterfowl and shorebirds.
Class II viruses have been divided into 11 genotypes (I to XI) with
genotypes V, VI, VII, and VIII being the predominant genotypes
circulating worldwide.
Among these, genotype VII viruses are particularly important given
that they have been associated with many of the most recent
outbreaks in Asia, Africa, and the Middle East

Antigenicity and immunogenicity
 Few antigenic variations
 Cell mediated immunity (Local immunity:
mainly IgA )
 Humoral immunity
 Antibodies against fusion protein
 Antibodies against HN protein : HI Ab
 Passive immunity of the chick

Kind of ND vaccines used for
immunization of chickens in Egypt:
A. Live lentogenic vaccines: Prepared
from naturally weak strains.
1. F. strain vaccine:
• It is used in chicks aged 1-10 days.
• Via eye dropping , nasal instillation ,
beak dipping
• Local prepared.

Kind of ND vaccines:
2. Hitchiner B1 vaccine:
• Used for individual vaccination (Eye).
• Massive vaccination (D.W) spraying.
• Used in chicks aged 1-10 days.
3. Lasota vaccine:( Colone, Avinew )
• It is more virulent strain than F & B1.
• It must used as a second vaccination
after the first one with either F or B1 .
• It’s used through DW., or spraying.

B. Live mesogenic vaccine:
• As Komarov vaccine, local prepared .
• Administrated only by intermuscular
I/M.
• Used for birds aged not less than 4-6
wks.
• Must be in good healthy condition and
not in production.

C. Inactivated vaccine (Dead vaccine):
• Egg propagated (velogenic virus) killed with
formaline with adjuvant.
• Administ.to chickens & turkeys I/M or S/C.
• Used for vaccination of chickens previously
vaccinated with ND live vaccine.
• It gives immunity after 14 days and the immunity
persist for 3-4 m in birds vaccinated at early age
and for 10-12 m in birds vaccinated at the age of
18-22 wks.
D. Recombonant vaccine :
Its live HVT vaccine Carring F gene of NDV, not
interfere with MDA, apply at 1 DO ,long protect.

Def.
 An acute, highly contagious catarrh
mainly of growing or mature chickens
usually in the cold winter time causing
upper respiratory tract disease (nasal
sinusitis), growth rate depression and
drop of egg production.

Etiology
Avibacterium paragallinarum (Haemophilus
paragallinarum).
H. paragallinarum is a gram-negative nonmotile
bacterium.
Culture on sheep blood agar is tiny dewdrop,
non-hemolytic colonies ,require both X-
(hemin) and V-(nicotinamide adenine
dinucleotide —NAD) factors for growth
A capsule may be demonstrated in virulent
strains.

Strain Classification
 The Page scheme was initially developed by
using a plate or slide agglutination test to
recognize the three serovars, A, B, and C .
However, the use of hemagglutination-inhibition (HI)
technology has been shown to be a much better
method for identifying the Page serovar of field
isolates.
 It is widely accepted that the three Page serovars
represent distinct ―immunovars,‖ since inactivated
vaccines based on any one Page serovar provide no
protection against the other two Page serovars

Susceptibility
 Infectious coryza is an acute respiratory disease of
chickens.
Mature ages are susceptible.

Mode of transmission
 The organism may be introduced by the airborne
route
Through direct contact Or indirect contact through
feed and water contaminated with nasal discharge.
 Infectious coryza occur frequently in fall and winter.
 Chronic or healthy carrier birds are the main source
of infection within 1—6 weeks after such birds are
moved from the brooder house to growing cages near
older groups of infected birds.
 Introduction of carrier replacement pullets or males
for spiking.
 Multiple-age groups.

Vaccines:
 Trivalent (A,B,C) thiomersal inactivated
bacterins are more effective than formalin one.
 A number of adjuvants have been shown to be
effec-tive for IC bacterins, in particular,
aluminum hydroxide gel, mineral oil, and
saponin
 108 colony-forming units/ml to be effective.
 In breeders, at 18 and 22 weeks of age into the
leg muscle.
 In layers, at 10 and 14 weeks of age.
 Significant immunity for about 9 months.

TREATMENT
 oxytetracycline , Erythromycin and sulphonamides are
commonly used antibiotics.
 It should be noted that drug resistance does develop
and hence the performance of antimicrobial sensitivity
tests is recommended.
 Strains of A. paragallinarum resistant to various
antibiotics did not carry plasmids.
 Relapse often occurs after treatment is discontinued
and the carrier state is not eliminated.

Clinical Forms of IB:
1.Respiratory Form (Classical)
2.Renal Form
3.Reproductive Form
4.Digestive Form
5.Muscular Form

IBV exists as scores, more than 360 serotypes.
Most differ from each other by 20 -50% of S1
amino acids
Classical strains:
Massachusetts (M41, H). Connecticut (Florida,
Clark 333, ArKansas 99), Georgia (SE17), Iowa
97, Iowa 609, New Hampashire and
variant strains:
Israel strain (Variant II)
QX strain
Dutch (D207, D3896, D3128, D212)
Delawar (JMK, Halte, Gray)
Australia T strain ( kidney lesions ).
These strain share common antigen by AGPT.
Show variable cross reactions with SNT.

Mode of infection and transmission
1. Air-borne disease. Infection occur through
respiratory tract and spread readily by direct and
indirect contact
(with 48 hr. between infected and susceptible one).
Carriers and vectors :
Recovered birds may shed the virus for 4-9
weeks (49 days) re-infection may lead to
persistence of infection and shedding of the virus
for long periods.

Incubation period
Naturally 3-10 days, experimentally 18-36 hrs. but natural spread about 36
hrs. it depend on:
Dose. Aerosol , Route of inoculation.
Symptoms and course :
The severity of the clinical and pathological picture of the disease
largely depend on :
Virulence and organ-affinity of strain .
Age and immune status of the birds.
General health condition and presence of complicating secondary or inter-
current infection, especially Mycploasma, E.coli, Haemophilus, Adenovirus,
etc.

Symptoms and course
In chicks under 6 wks age :
A: Respiratory form
Cause mortality of 5 to 10% up to 50%. With depression, ruffling, loss of
appetite, gasping, rales, coughing, sneezing and wet eyes.
Course of disease is usually 3-6 days.

Catarrhal trachitis , bronchitis and pneumonia are common. Red
and yellowish caseaus plugs may be found in the lower part of the
trachea and bronchi, Rhinitis and air-sacculitis are sometimes
present.
(Pericarditis, Peri-hepatitis, air-sacculitis in a complicating by
inter-current MG, MS and secondary E.coli infection)
PM Lesions

‫ّالؼالج‬ ‫الْقبيخ‬
‫انتىصُاخ‬‫تها‬ ‫انعًم‬ ‫َدة‬ ً‫انت‬:
ٍ‫انذواخ‬ ‫عُاتش‬ ً‫ف‬ ‫انالصيح‬ ‫انصحُح‬ ‫االحتُاطاخ‬ ‫يشاعاج‬(ٍ‫ي‬ ً‫انصح‬ ‫انتخهص‬
‫انُافمح‬ ‫وانطُىس‬ ‫انسثهح‬)
ٍُ‫انتحص‬:
‫يصش‬ ً‫ف‬ ‫انًىخىدج‬ ‫انحمهُح‬ ‫انعتشج‬ ‫وتصُُف‬ ‫عضل‬
ً‫ف‬ ‫وَظائشها‬ ‫يصش‬ ً‫ف‬ ‫انحمهُح‬ ‫انًعضوالخ‬ ٍُ‫ت‬ ًُُ‫اند‬ ‫انتماسب‬ ‫يذي‬ ‫دساسح‬
ًُُ‫اند‬ ‫انثُك‬.
‫يغاَشج‬ ‫تعتشج‬ ‫االصاتح‬ ‫ظذ‬ ‫انتًُُع‬ ً‫عه‬ ‫لادسج‬ ‫انًتىفشج‬ ‫انهماحاخ‬ ٌ‫ا‬ ‫تحذَذ‬
‫انعًهُح‬ ‫انتدشتح‬ ‫طشَك‬ ٍ‫ع‬ ‫رنك‬ ٍ‫ع‬ ‫عاخضج‬ ‫او‬ ‫خذَذج‬(ٍ‫انتًُُع‬ ‫انتصُُف‬
Protectotype)‫انهماحاخ‬ ٍ‫ي‬ ‫وعذد‬ ‫يصش‬ ً‫ف‬ ‫انحمهُح‬ ‫انًعضوالخ‬ ٍُ‫ت‬
‫انًستخذيح‬.
‫أو‬ ‫انشش‬ ‫طشَك‬ ٍ‫ع‬ ً‫ه‬ ‫انفُشوط‬ ‫ظذ‬ ٍُ‫نهتحص‬ ‫طشق‬ ‫أفعم‬ ٌ‫أ‬ ً‫عه‬ ‫انتأكُذ‬
ٍُ‫تانع‬ ‫انتمطُش‬(‫تعذ‬ ‫ثى‬ ‫َىو‬ ‫عًش‬14‫َىو‬.)

Causes of failure
Eye drop : 98-100%
At 10 days PV
DW vaccine: 56% protection
―10 day PV‖
Hand spray at hatchery : 32%
(2wks PV), 86% (3 wks PV).
Automatic spray : 93-97% .

Infectious Laryngotracheitis (ILT) is a viral upper respiratory tract infection of
chicken which produces severe production losses due to mortality of infected
pullets and adult birds and/or decreased weight gain and egg production.
Severe epizootic forms of ILT show a great respiratory distress, gasping,
expectoration of bloody mucus, and high mortality.
Mild forms of infection, sometimes enzootic, are characterized by mucoid
tracheitis, sinusitis, unthriftiness, and low mortality.
History:
ILT was reported in the USA in 1925 and its earliest recorded
occurrence in the UK was in 1935 . It is now recognized worldwide .
Introduction

ILT virus is a member of the family Herpesviridae in the subfamily
Alphaherpesvirinae . The virus is taxonomically identified as Gallid
herpesvirus 1 .
• Characteristics:
• INIB: Intranuclear inclusions in the trachea and on the
chorioallantoic membrane
• Types: only one, differentiated by PCR, Variation in virulence
• Cultivation: pocks on the CAM and Syncytia in cell cultures
• Latency: ILT virus becomes latent like other herpesviruses
Etiology:

ILT virus strains appear to be antigenically
homogenous based on serum-neutralization
,immunofluorescence tests and ELISA .
Naturally occurring ILT virus strains vary in
virulence from highly virulent strains that
produce high morbidity and mortality in
exposed chickens to strains of low virulence
that produce mild to in-apparent infection .

Susceptibility:
-Chicken is the primary natural host of ILT and
occasionally pheasants and guinea fowl
-All ages are susceptible ,the most characteristic
signs are observed in adult birds.
-In general males are more susceptible than
females and the heavier breeds more susceptible
than light.

Mode of infection :
Natural portals of entry for ILT virus are through the upper
respiratory and ocular routes .
Ingestion can also be a mode of infection although exposure of
nasal epithelium following ingestion is required with this route .
Transmission:
Horizontal transmission by
Direct contact between infected birds with susceptible birds .
Indirect contact through contaminated equipments and buildings
with aerosol or expectorant of infected birds .
Mechanical carriers such as personnel ,wild birds ,vermin ,cats
and dogs .
Recovered birds and even birds given attenuated live vaccines
,the birds become carriers .

• Horizontal spread:
in droplets from infected birds
- spread often slower than other
respiratory diseases e.g. IB, ND.
- other agents may exacerbate
disease

Latency:
ILT virus or vaccine becomes latent and
can be re-excreted intermittently for many
weeks
reactivation due to stress, onset of lay, etc.

Incubation period:
6-12 ds. following natural exposure
.

Gross lesions:
Lesions may be found in the conjunctiva and throughout the
upper respiratory tract of ILTV-infected chickens ,but they are
most consistently observed in the larynx and trachea .
A) In mild forms of ILT ,gross lesions may consist only of
conjunctivitis ,sinusitis and mucoid tracheitis .
B) In severe forms of ILT ,mucoid inflammation is observed early
in infection with degeneration ,necrosis and hemorrhage
occurring in later stages .
-In some cases ,severe hemorrhage into the tracheal lumen may
result in blood casts or blood may be mixed with mucus and
necrotic tissue .
-Diphtheritic changes commonly are seen as mucoid casts that
extend the entire length of the trachea .

Modified Live attenuated vaccines
Used in areas of high risk
Often where used routinely – ‗afraid to stop‘
• Application methods: ED, spray or DW
• Live vaccines can become latent
• Beware of adding vaccinated or recovered
birds to a susceptible flock
Vaccination

Vaccination program :
Layers flocks generally are vaccinated twice before
the onset of egg production ;vaccines typically are
administered by eye drop at approximately 7 wks.
of age and again at approximately 15 wks.
(by eye drop ,spray or drinking water.)

Live attenuated ILT vaccines provide immunity when
applied via intranasal instillation , eye drop, and orally
through drinking water.
However, application of ILT vaccines by eye drop method
appears to be more protective than application by water or
spray.
Most vaccines when given by eye drop method had
lower mean microscopic lesion scores and higher
ELISA titers after one vaccination.

Fortunately, ILT is a slowly spreading (long IP) ,
controllable disease. If a diagnosis of ILT is
obtained early in an outbreak, vaccination of
unaffected birds may induce adequate protection
before they become exposed.
Emergency vaccination

The infection results in elevated
mortality in flocks, lower egg
production in commercial laying and
breeder flocks, degraded broiler
growth rate, and a marked reduction
in carcass quality and elevated
condemnation at processing.
Healthy and sick broilers, layers, and
breeders showed the incidence of APEC
infection to be 17.7%, 38.6%,
and 26.9%, respectively. Resistance
to antibiotics was also found to be high

43% of broiler
carcasses condemned
at processing had
lesions of
colisepticemia

Definition and Synonyms
Colibacillosis refers to any localized or systemic
infection caused entirely or partly by avian
pathogenic Escherichia coli (APEC), including the
following forms:

1. Colisepticemia (hemorrhagic
septicemia) S
2. Coligranuloma (Hjarre’s disease) S
3. Air sac disease S
(chronic respiratory disease, CRD)
4. Swollen-head syndrome L
5. Venereal colibacillosis (Acute
Vaginitis) L
6. Coliform cellulitis L
(inflammatory or infectious
process, IP)
7. Coliform peritonitis L/S
8. Coliform salpingitis L/S
9. Coliform orchitis L
10. Coliform osteomyelitis S
11. Coliform synovitis S (including
turkey osteomyelitis complex)
12. Coliform panophthalmitis S
13. Coliform omphalitis/yolk sac
infection L
14. Coliform enteritis L

Antigenic Structure and Toxins

Antigens
H-antigens
= Flagellar
K-antigens
= Capsular
F-antigens
= Pilus
O-antigens
= Somatic

Antigens
O-antigens
• Somatic (lipopolysaccharide or endotoxin released at cell lysis)
• often used in serotyping and antigenic identification
H-antigens
• Flagellar (proteins not often used in antigenic identification)
K-antigens
• Capsular (polysaccharides associated with virulence)
• Pilus (involved in attachment
to cells)F-antigens

• Serotypes of E. coli
are classified
according to the
Kauffmann scheme
Currently there are
approximately
180 O, 60 H,
80 K and 17F
antigens
• In most serologic
typing schemes only
the O and H antigens
are determined (e.g.,
O157:H7).
Antigenic structure

Swollen Head Syndrome.
 Swollen head syndrome (SHS) is an acute to subacute
cellulitis involving the periorbital and adjacent
subcutaneous tissues of the head.
 Usually occurs following upper respiratory viral
infections (e.g., avian metapneumovirus, infectious
bronchitis virus) & Ammonia aggravates the disease

Pericarditis and green
discoloration of the liver
Salpingitis in a young bird caused by E. coli.
Large caseated masses distending the oviduct
(salpingitis).
Goose breeder with acute peritonitis. Yolk in the
peritoneum.

Omphalitis
(Salmonella , Pseudomon ,
Streptococus facaeum, Proteous(

SHS
(MG, IB, AI, IBD or high amonia
as preliminary infection)

Panophthalmitis
(amonia, Aspergillosis)

Treatment
 Sensitivity test.
 Ampicillin, fluoroquinolones, chloramphenicol,
oxytetracycline, chlortetracycline, neomycin, gentamicin,
ormethiprim-sulfadimethoxine, nalidixic acid,, polymyxin
B, spectinomycin, streptomycin, sulfa drugs, apramycin,
neomycin,.
 monensin (anticoccidial) in feed reduced colonization with
E. coli O157:H7.

Vaccination
Types of Vaccines
 A variety of vaccines and vaccination methods have
been developed, including passive and active
immunization:
1. Inactivated vaccines
2. live vaccines
a. Recombinant vaccines
b. Subunit vaccines
3. Immunization against specific virulence factors.

Mutant O2 and O78 APEC with deletions of the genes
cya or crp, which are involved in energy production,
were used as a spray vaccine to immunize broiler
chickens.
Similarly, strain O78 mutants with deletions of galE,
purA, and aroA genes were found to be safe and
immunogenic, but provided only moderate protection
against homologous challenge with no protection
against heterologous challenge

Def.
 Ornithobacterium rhinotracheale infection is a contagious
disease of birds mainly turkey and chickens that causes
respiratory distress, mortality, and decreased growth.
 The severity of clinical signs, duration of the disease, and
mortality are extremely variable and are influenced by
environmental factors, such as poor management, inadequate
ventilation, high stocking density, poor litter conditions, and
poor hygiene.
Ornithobacterium
rhinotracheale
ORT

Economic importance of ORT in turkey industry
• increased mortality
• increased condemnation rates,
• decreased growth,
• decreased egg production,

Transmission
O. rhinotracheale is highly contagious:
• Infection by inhalation.
• Transmitted horizontally by direct and
indirect contact through aerosols or
drinking water.
• Vertical transmission occurs as ORT
was isolated from ovaries, oviduct,
hatching eggs, infertile eggs, dead
embryos, and dead-in-shell poults and
chicks.

Serotypes
 18 serotypes (A- R).
 Serotype A was the most prevalent serotype
among chicken isolates (94%) and turkey
isolates (57%) but not in USA and South
Africa.
 Serotype C is prevalent in chickens and turkey
in South Africa and USA.

Colony Morphology
 On blood agar, very small, non-hemolytic
colonies circular, gray to gray-white, sometimes
with a reddish glow, and convex with an entire
edge.
 ORT is a gram-negative, non motile, highly
pleomorphic, short, plump rod-shaped, non
sporulating bacterium.
 No pili, no fimbriae, no plasmids, or specific
toxic activities have been reported.

 Sprayed, live temperature-sensitive mutant of
O. rhinotracheale vaccine.
Treatment
 Amoxycillin, ampicillin, Florfenicol.

INFECTIOUS BURSAL DISEASE
(IBD)
GUMBORO DISEASE

Definition
• An acute, very contagious, viral disease
of young chickens characterized by
destruction of lymphocytes in the Bursa
of Fabricious and, to a lesser extent, in
other organs.

Etiology
• Infectious bursal disease virus is a member of the Birnaviridae family,
named for the bi-segmented double stranded RNA nature of the genome of
its members.
• The family has 4 genera designated Aquabirnavirus, whose type species is
infectious pancreatic necrosis virus (IPNV) of fish, molluscs, and
crustaceans; Blosnavirus, whose type species is blotch snakehead virus or
BSNV; Avibirnavirus, whose type species is IBDV, which infects birds; and
Entomobirnavirus, whose type species is Drosophila X virus, which infects
insects.

Viral proteins
RoleProtein
Encapsidation of viral particle
VP1
RNA dependant RNA
polymerase
(Small amount in virus
capsids)
Contain antigenic region responsible for
Serotype specific
Elicit neutralizing antibodies
(responsible mainly for protection)
VP2
Main capsid protein
Morphogenesis of the virus
VP3
Other major structural
protein nit exposed at the
surface
Viral protease (maturation of VP2 trimming peptides
during virus assumbly)
VP4
Viral relaseVP5

 IBD virus non-enveloped and resistant to
environmental factors
 Can persist for months in contaminated houses
as once a house is contaminated with IBDV,
the disease tends to recur.
 Viruses exhibit different degrees of
pathogenicity, variants are recognized

Antigenic types Pathotypes
Serotype 1
A: Classical (standard) strains:
• Mild
• Intermediate
• Intermediate plus
• Very virulent or hyper virulent
(VVIBDV) (Hot strain)
B: Variant: (antigenically different
from classical) and mostly low
pathogenic causing only
immunosuppression without
specific lesions
Serotype 1 (Pathogenic)
Serotype 2 (Apathogenic)
 IBDV serotypes 1 and 2
share only 30% antigenic
relatedness

• Strains of IBD follow one of two courses of
disease depending on the age at which
chickens are infected
• Subclinical course
• Clinical disease

Variant Strains of IBD
-Subclinical Form-
 Infection of susceptible chickens less than 2 weeks
of age when chickens are exposed to IBDV during
the first two weeks post hatch and have sufficient
maternal antibody at time of infection to prevent
clinical disease but not viral replication in the
bursa.
 No clinical signs, No peak mortality as evidenced
with clinical IBD, but permanent and severe
immunosuppression
 More economically important form
 Majority of field infections are subclinical

 Subclinical form- Perminant immunosuppressive
reduced antibody response to vaccination
strong post-vaccine reactions
 Increased susceptibility to concurrent or
secondary disease as E. coli, Mycoplasma and
NE
 Inability to clear vaccine virus

Varian
t
strains
Direct
bursal
atrophy

Standard Strains of IBD
-Clinical Form-
 Infection of susceptible chickens 3-6wks
weeks of age:
 Sudden onset, rapid increase in mortality
 Clinical signs include ruffled feathers, diarrhea,
vent pecking, dehydration, trembling,
depression, transient immunosuppression

Clinical Signs
1. Anorexia, depression and ruffled feathers.
2.Whitish or watery diarrhoea.
3.The earliest signs is self vent picking and soiled vent feathers.
4. Dehydration and trembling.
5. In terminal stages of the disease, subnormal temperature,
severe prostration and finally death.

Morbidity &
Mortality
In susceptible flocks, there is
high morbidity rate usually
approaching 80%.
Mortality may be nil but can be high as 20-
30%
and usually begin at 2nd day post infection and
peaking and receding in a period of 5-7
days.

Gross Lesions
Changes in cloacal bursa
2nd day post infection ----- bursa has
gelatinous yellowish transudate covering
serosal surface with prominent longitudinal
striations.
By 3rd-4th day ----- bursa is double in size and
weight (due to edema and hyperemia).
By 5th day -------- bursa returns to its normal
weight but it continues to atrophy
From 8th day forward --------- bursa is
approximately 1/3 its original weight.
Mortality rate
Slightly higher
Double
Slightly lower
Normal

2. Dehydration.
3. Haemorrhages in mucosa at junction of
proventriculus and gizzard.
4. Haemorrhages in thigh and pectoral muscles.
5. Increase mucous in intestine.
6. Spleen and liver slightly enlarged.
7.Pale kidney ,nephritis and ureter distended
with urates.

Vaccination
1. Live IBD vaccines: (1-14 days)
Divided according to virulence of strains:
Mild strains
Intermediate
Intermediate plus
Hot strains
applied in drinking water, eye drop.
2. Oil-adjuvant, killed IBDV vaccines:
Applied by injection S/C or I/M and used to booster
or prolong immunity in breeder flocks.

In ovo vaccination
 A more recent concept for the vaccination of
chickens for IBD and other agents is in ovo
vaccination at 18 days of incubation.
 In ovo is a labor-saving technique and may provide
a way for vaccines to circumvent the effects of
maternal antibody and initiate a primary immune
response.
 The injected material is a live IBD vaccine, either
alone or in combination with an anti-IBDV antibody
to form immune complexes

Recombinant vaccines
 live recombinant virus vectors expressing IBDV
immunogens (VP2) as:
 Herpes virus of turkey (HVT) Marek‘s disease
virus
 Fowlpox virus
 Chick embryo lethal orphan (CELO) virus
(Adenovirus)
 Newcastle disease virus
 Baculovirus

 Vaxxitek antigen = Faragher 52/70
 Old classical strain
 Transmune strain = Winterfield 2512 (= IBD
Blen)
 Very hot strain
Recombinant vaccines
Immune-complex vaccines

Control of outbreak
*Supportive and symptomatic treatment :
1. Diuretics to increase efficiency of kidney and to prevent
precipitation of urates .
2. Immunostimulant as vitamin E and levamisole .
3.vitamin K (for hemorrhage).
3.give coarse of antibiotic to prevent 2nd ry bacterial infection
(but it‘s contraindicated in case of nephritis).

Other immun-suppressive diseases

‫نفُشوط‬ ً‫انًُاع‬ ‫انتثثُط‬H9N2
1. Atrophy of bursa of Fabricious and
thymus gland
2. Ciliostasis and affect BALT
3. Decreased antibody production

Infections caused by non-motile
Salmonella serotypes (Salmonella entrica
subspecies entrica serovar pullorum
gallinarum)
PD can cause 10-80% mortality during
the first 2 weeks.
FT can cause mortality as high as 26% in
chicks during the first month of life.

Infections caused by motile Salmonella
serotypes are called paratyphoid (PT)
salmonellae.
More than 2500 serotypes (of which 30%
are caused by S. enteritidis and S.
typhymurium).

 Salmonella infections cause:
High mortality rate especially in young chicks
Drop in egg production
Decreased fertility and hatchability

Nephritis
(IBD, ANV, Ochratoxins, High protein ration)

Heart nodules
(MD, Coligranuloma and Aspergillosis)

NE Caused By C. perfringens is an
anaerobic, spore-forming, large Gram-
positive rod, which is motile by pili.
It is commensally live in the intestinal
tract (lower gut & caecum ).
There are five different types of CP {A-E}
where A and C is mainly responsible for
NE in broilers.

C. Perfringens Infection causes
1. Impaired FCR.
2. Reduced Weight Gain At Slaughter.
3. Reduced The Average Of Farmers Profit With 33% With
High And Low Levels Of The Disease.
4. Increased Number Of Carcass And Liver Condemnation At
Poultry Processing Plants.

Pre-disposing factors For NE:
 Concurrent coccidial infections with scores 2-3
 Removal of antibiotics growth promoter
 Long anticoccidial withdrawal periods.
 Feed and litter contamination with Clostridial spores have been
incriminated as a source of infection.
 Diet is believed to be an important:
 Change Viscosity and PH (High level of wheat & Barley
increasing SNSPS)
 High Protein in ration
 High level of animal by products i.e fish meal

 Direct damage to intestinal mucosa (coccidia
infection, mycotoxicosis, bacterial over growth).
 Immuno-suppressive such as: CAV, IBD, M.D.
 litter high in fiber content, feeding programs e.g.
skip a day starvation, overstocking).

Susceptibility:
NE has been reported in many bird species but
mostly in broilers 2-6 wks), layer pullets, adult
layer, breeders and turkeys.

 Pseudo-membranes covering the entire
mucosa of large segments of SI which
resemble a coarse yellow coating.
Cholangiohepatitis:
 Most common lesion CC by inflammation
of bile tree (Intra-hepatic part most
frequently).

1. Gross intestinal lesions
2. Present of liver lesions
3. Microscopically exam of gut smears for coccidia.
4. Bacteriological examination: gut content should
contain at least 1 million often 100-1000 million
CP/gm)
Differential diagnosis

Treatment of NE
 Treatment of NE outbreaks can be
effectively treated by administration of:
 Ampicillin , Amoxicillin ,Lincomycin,
Bacterin, and Streptomycin.
 Metronidazol

 Species Specific (no cross-immunity exists
between species of Eimeria ).
 Host specific.
 Tissue specific.
 Simple, short and direct life cycle.
 High reproductive potential of coccidia in
poultry intensifies the potential for severe
outbreaks of disease in the modern poultry
house (New house disease).
 It is a self limiting parasite.
Characteristics of coccidian parasite:

Classification:
- Chickens coccidiosis: I – Intestinal II- Caecal
I - Intestinal. coccidiosis
A- Anterior E. acervulina
E. praecox
B- Middle E. necatrix
E. maxima
C- Posterior E. brunetti
II- Caecal coccidiosis
E. tenella

Clinical signs: The Common Rule Says That:
The species We Don't See Cause More
Damage and More Loss.
1- diarrhea from (catarrhal to
hemorrhagic,...etc.)
2- dehydration.
3- death.

Significantly damaged and therefore lesser
absorbing ability of the intestine membrane.
All of this leads to the weakening of the
animal, a poorer usability of food and
poorer conversion, flock disintegration and
growth retardation, lesser body weight, poorer
production results.

Diarrhea and dehydration are very
common and depending on the type of
coccidiosis as well as traces of blood in or
bloody feces with consequential anaemia,
as well as death of infected units where
mortality may be expressed in a very
significant percentage.
Coccidiosis is primarily a disease affecting
young animals.

E. acervulina & E. maxima:
Poor weight gain, high morbidity,
diarrhea, and sometimes mortality.
There is often extreme emaciation,
ruffling of feathers , anorexia.
Killers (E. tenella & E. necatrix):
bleeding, high morbidity and
mortality, lost weight gain, emaciation,
loss of skin pigmentation.

P.M. lesions
Lesions of the intestine can vary from mild enteritis one
score (+ve) to
severe necrotic or hemorrhagic type scores (+++ve) and
characterized
by :-
1- sever inflam. in specific location according to
Eimeria sp.
2- thicken of intestinal wall.
3- whitish yellow plaques (oocysts).
Caecal coccidiosis may produce ballooning of the cecal
pouches, which then fill with blood. A later stage involves
cecae filled with material of cheesy consistency, streaked
with blood (contains non sporulated oocysts) (whitish
yellow plaques) or (caecal cords).

Lesions can often be seen from the serosal
surface of the small intestine.
The intestinal mucosa may at first be thin
and covered with elongate white plaques,
arranged transversely.
The intestine may be pale and contain
watery fluid.
E. acervulina

The intestine may be flaccid and filled
with fluid, and the lumen often contains
yellow or orange mucus.
This condition has been described as
―ballooning.‖
E. maxima

E. necatrix
older birds such as brooder pullets or
layer pullets 9—14 weeks old.
The intestine often is dilated to twice its
normal size (ballooning), and the lumen
may be filled with blood and fluid.

I - Correct the managment:
- avoid humidity.
- avoid over crowdness
- provide good ventilation.
- proper temp.
- Eradication of rodents, arthropods (vectors).
- Disinfectant of the visitors, workers & shoes.
- Separate the old from the young. birds
- Control other disease.
- through cleaning & disinfection before each new flocks.
- periodical removal of litters
wet letter should be changed either completely or partially as
possible. Wet areas are found
around drinkers, in corners or beside walls and … etc.

II- Destruction of oocyst
- good hygiene
- good disinfectant
Ammonia fumigation
or Ammonia solutions
or Sodium hydroxide.
or Calcium oxide
III- Raise the vitality of the birds:
- good balanced rations.
- supplemented especially by vit K & vit A.
- sufficient amount of ration.

IV – Feed additive compounds:
- Used as protective coccidiostate:
-Add from the first day of age to the end of the broilers flocks
at ration and add from the first day of age to 12-16 weeks of
age at ration in layers flocks.
-Use for non diseased birds & not used as treatment. e.g.:
1- Chemicals coccidiostate
Active principle
1- Halofuginon
2- Rubanoed
3- Dicelazoril

2- Inophores coccidiostate
Active principle
1- Monenzin
2- Salinomycin
3- Lasalocid
4- Maduramycin
5- Semduramycin
- Coccidiostate permit descend of some oocysts which lead to
partial immunity
There are two main problems with chemotherapeutic approach to
controlling coccidiosis, the emergence of drug resistance (which
may be developed after repeated uses of the same drug) and
residues. This problem is usually met by changing the anticoccidial
drugs overcome the drug resistance as following:

Programs for coccidiosis control:
1- Continous use of single drug:
using one particular anticoccidial in the feed from first day till withdrawal period
2- Shuttle programs (‫الواحدة‬ ‫الدورة‬ ‫خالل‬ ‫الكوكسيديا‬ ‫مضادات‬ ‫تبادل‬ )
Consists of starter medication, using one particular anticoccidial in the feed
usually for the first 3 weeks of growth, followed by a change to another
anticoccidial in the grower feed for the finishing period.
3- Rotation programs ( ‫تبادل‬‫مضادات‬‫الكوكسيديا‬‫بين‬‫الدورات‬ ) :
using one particular anticoccidial in the feed for 2 cycles then change to
another.

 Used for breeders and floor reared layers:
Natural wild type vaccine:
Coccivac,Immucox.
Attenuated vaccine:
Livacox, or Paracox.
Vaccination

Immunogenicity of different species:
Depending on the coccidian species considered, immunity
will develop after one single exposure to the parasite or
several exposures to the same species as shown in the
following table:
Species No. of Exposure to achieve
Immunity.
E. maxima 1
E. Praecox 1
E. brunetti 1-2
E. acervulina 2-3
E. mitis 2-3
E. tenella 3-4
E. necatrix 4-5

VI - Vaccination:
- Administration via feed 3-5 days
or spray (Cabin) 1 day old
or eye of nasal drop 1 day old
- Immunity after 3-4 weeks

Precautions after vaccination:
-Never use a medication which affect any stage
of Eimmeria sp.
-Never change the litter for one month following
vaccination.
Examination for the chicks periodically to be sure
from the presence of oocysts & absence of lesion
scores.

Mycotoxicosis & their effect on poultry
industry

Mycotoxicosis
Mycotoxins are secondary metabolites produced by
fungi that can enter the human and animal diet
through direct or indirect contamination of cereals
and grains.
There are more than 350 type of mycotoxines

Mycotoxin Fungi Produced
Commodities
affected
Aflatoxin(B1,B2,G1,G2)
Aspergillus flavus
Aspergillus parasiticus
Corn, cotton seed,
peanuts, soya
Ochratoxin (A, B, C)
Aspergillus ochraceus
Aspergillus nigr
Penicillium verrucosum
Wheat, barley, oats,
corn, others
Trichothecenes
(DON, T-2, DAS, etc)
Fusarium graminearum
Fusarium culmorum
Corn, wheat, barley
Zearalenone Fusarium graminearum
Corn, wheat, barley,
grass
Fumonisin
Fusarium verticillioides
Fusarium proliferatum
Corn
Moniliformin Fusarium moniliforme Corn
PR toxin, patulin Penicillium roqueforti Silage, Grass

Species
Single oral doseLD50 mg
kg -1 bodyweight
Rabbit 0.30
Duckling
(11 day old)
0.43
Chicken 6.30
Effect of bird species on toxicity of
aflatoxin B1

Type of bird Age (days) LD50 (mg/Kg Bwt)
Ducklings 3 0.5
Broiler chicks 1 2.14
Leghorn Chicks 1 3.3/3.9
Leghorn Chicks 3 3.4
Turkey poults 1 4.63
Turkey poults 3 5.9
Japanese qual chicks 3 16.5
Effect of age on toxicity to LD50 of ochratoxin A (after single oral
administration).
Type of bird Age (days) LD50 (mg/Kg Bwt)
Ducklings 3 0.5
Leghorn Chicks 1 3.3/3.9
Turkey poults 3 5.9
Japanese qual chicks 3 16.5
Effect of age on toxicity to LD50 of ochratoxin A (after single oral
administration).

Level producing
Immunodepression
Regulations
UE - USA
Mycotoxins
5 ppb< 20 ppbAflatoxin
2ppb0-2 ppbOchratoxin
100 ppb< 500 ppbToxin T-2
< 500 ppbZearalenone
1000 ppb< 5000 ppbFumonisin
200 ppb< 1000 ppbVomitoxin(DON)
MYCOTOXIN TOLERANCES
(Synergism)

level , synergism & duration
animal species , breed, sex, age, general health,
immune status
farm management( storage, Temp., & RH / infections )
• toxin-,
• animal-
• environmental-
Factors influencing Mycotoxines
depend on:
related factors

Growth depression .
Increased mortality .
Increased susceptibility to disease .
Decreased serum protein .
Impaired blood coagulation (Decrease vit K
absorption) .
Fatty liver .
Weakened bones (Decrease vit D absorption) .
Poor nutrient absorption .
Principle effects of aflatoxin in
broiler

1. Pale bone marrow.
2. Regression of the bursa of Fabricius.
3. Mycotoxins can cause damage to
mucosae with which they come in
contact.
4. Gizzard erosions.
5. Enteritis of variable degree may be
seen.

 Produced in moderate and colder climates.
 It is stored in fatty tissues.
 OTA is also known as a potent immunotoxic, teratogenic,
and carcinogenic mycotoxin.
 In addition, OTA ingestion induces intestinal injuries,
including inflammation and diarrhea.
 It is nephrotoxic.
 Immunosuppressive: decrease immunoglobulin production
and causes lymphocytopenia at 4 ppm.
Ochratoxin

Citrinin:
 Nephrotoxic.
 Na and K increased excretion.
 Inbalance in the minerals and salts PPT of uric
acid crystals inside the kidneys.
 At the final stage the nervous signs appear,
(convulsions and death).

Trichothecenes:
Mytotoxins produced by Fusarium sp.
Includes more than 100 types.
T--2 toxin LD50(4
mg/kg),
HT-2 toxin
Di-acetoxy-scirpenol
Deoxy-nivalenol (DON)
LD50(27 mg/kg)
Neural toxicity
Necrosis, odema,
hemorrhage of intestinal
tract

Prevention And Control Of
Mycotoxicosis

1. Quality control of the raw material all the
way through feed mill, delivery, storage
bins, at the farm, feed through, litter
condition in poultry houses.
2. Storage time must be reduced to minimum
esp., in starter feed.
3. Feed bin & handling equipment must be
kept clean & disinfectant with 10% clorax.

• Decontamination for mold & mycotoxins
infestation.
-Ammoniation .
-Cleaning “ all visible mold areas”.
-Heating or roasting of feedstuffs.
-Adding toxin binders (HSCAS) to feedstuffs.
• Using of mold inhibitors (which inhibitor
should be used & at what conc.?

Propionic acid was the only compound
exhibiting cidal action.
Ca. propionate had essentially no effect on mold
growth .
Sod. Propionate had essentially mild activity
towards mold growth.
The failure of these two compounds to exhibit
marked anti fungal activity may be
attributable to PH of medium since
dissociation of these salts is PH dependent
Mode of action of mold inhibitors:

Mycotoxin binders:
An effective binder or sequestering agent is one that prevents or
limits mycotoxin absorption from the gastro-intestinal tract of
the animal.
In addition, they should be free from impurities and odours.
Be aware that not all are equally effective. Many can impair
nutrient utilization and are mainly marketed, based on in-vitro
data only.

Mycotoxin binding is achieved through both:
1- Physical adsorption
Relatively weak bonding through hydrogen bonding
2- Chemical Adsorption (Chemisorption):
It is a stronger interaction which involves ionic or
covalent bonding.

Inorganic binders
Organic adsorbents
Inorganic binders
Inorganic mycotoxin binders are silica based polymers.
Examples could include:
zeolites
bentonites
bleaching clays from the refining of canola oil hydrated
sodium calcium aluminosilicates (HSCAS) diatomaceous
earth numerous clays
There are two types of chemical mycotoxin
adsorbent/binder:

Extracts of yeast cell wall
Such materials are biodegradable but can, in some
cases, also be vectors of mycotoxin
contamination.
Benefits of yeast cell wall are low inclusion, high
surface area and certainly no toxic contaminants.
The efficacy of glucomannan-containing yeast
products as mycotoxin adsorbents in feeds has
been investigated globally with several studies
with all animals.
Organic Adsorbents
Organic mycotoxin adsorbents are carbon based
polymers.

 Bio-Transformation
Bio-Agglutination
Bio-Degradation
How dose Bio-mycotoxin work against
mycotoxins:

Bio-Transformation:
Bio-Transformation is one of four processes involved in
toxicokinetics

A substance biotransformed into a more toxic
metabolite (bioactivated) is a greater hazard
than a substance that is biotransformed into a
less toxic or even non-toxic metabolite
(detoxified).
Bio-Transformation:

Some specially selected strains of
Bacillus subtlus,
Lactobacillus,
S.faecium,
S. cerevisiae
and other technologies that Bio-
Transform, (detoxify) mycotoxins.
Bio-Transformation:

The process by which toxic
or
pathogenic
substances ―stick‖ to long chain
olygosacharide molecules
Bio-Agglutination:

Degradation via enzymatic activity
Bio-degradation:

ٍُ‫انتحص‬ ‫تشايح‬ ‫اعذاد‬
.1‫ثٌْػيِب‬ ‫االًفلًْشا‬.
.2ٓ‫الوؼذ‬ ٔ‫الشؼج‬ ‫االلتِبة‬.
.3ّ‫الجوجْر‬.
.4‫الٌيْكبطل‬.

‫الوزظيخ‬ ‫االصبثبد‬ ٔ‫ف‬ ‫التحكن‬
.1‫ثذقخ‬ ْٓ‫الحي‬ ‫االهبى‬ ‫ّطبئل‬ ‫اتجبع‬.
.2‫الصحيخ‬ ‫ّالؼْاهل‬ ‫ثبلتزثيخ‬ ‫االُتوبم‬.
.3‫جيذا‬ ‫ّاالدّيخ‬ ‫ثبلتحصيٌبد‬ ‫االُتوبم‬.
.4‫الوزظيخ‬ ‫للوشبكل‬ ‫الظليوخ‬ ‫التشخيص‬ ‫ّطبئل‬ ‫اتجبع‬.

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