Final Poultry Disease Coulored Demo

‫ حقوق البيع ترجع للكاتب‬...
‫نسخه عرض غير مخصصه للبيع‬
Poultry and rabbit diseases

( viral and parasitic diseases part )
Dr/Muhammed Abd-Alfattah Muhammed
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‫ حقوق البيع ترجع للكاتب‬... ‫نسخه عرض غير مخصصه للبيع‬
Table of the contents

title page
introduction 4
Main points of viruses study 7
Chapter 1 : Avian immunology and vaccination concepts 11
Chapter 2 : Avian parasitic disease :
External parasites of poultry 26
Nematodes 27
cestodes 30
Avian coccidiosis 32
Chapter 3 : Dis causing skin lesions
POX virus (PV ) 39
Marek’s virus (MDV ) 44
DD of Dis causing skin lesions. 50
Chapter 4 : Dis causing nervous manifestation
Avian encephalomyelitis (AEV ) 52
Avian influenza (AI) 55
Newcastle disease(NDV ) 60
DD of Dis causing nervous manifestation 65
Chapter 5 : Dis causing GIT disturbance
REO virus 67
THE + ADENO introduction 70
DD of Dis causing GIT disturbance 73
Chapter 6 : Diseases cause immune-suppression and hemorrhagic syndrome
Inclusion body hepatitis .( IBH ) 75
Gumboro (IBDV ) 76
Chicken anemia virus (CIA –CAV ) 80
DD of Diseases cause immune-suppression and hemorrhagic 83
syndrome
Chapter 7 : Dis cause respiratory manifestation
Avian pneumovirus (APV ) 85
Egg drop syndrome( EDS ) 88
Infectious bronchitis ( IB ) 90
Infectious laryngotrachitis ( ILT ) 94
DD of Dis cause respiratory manifestation 97
DD of disease affect egg production and hatchability 98
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Chapter 8 : Rabbit viral and parasitic disease

Viral hemorrhagic disease(VHD) 102
Myxomatosis 104
Coccidiosis + POX 105
Arthropode + worms 106
Microsporidium 107
Chapter 9 : Water fowls viral disease
Duck viral hepatitis (DVH) 109
Duck viral enteritis ( DVE ) 113
Hemorrhagic Nephritis Enteritis of Geese 115
Goose parvovirus 116
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Introduction
Poultry market considered the biggest animal production ,market in
Egypt , as it provides relatively cheap white meat , and eggs .
Millions has been invested in poultry market , as Egypt was the first
poultry production country in Africa and all Arabian countries until
2008 , where the diseases increased and totally changed the production
system of the poultry in the whole country .
The biggest threat then wan Avian influenza which we almost had a
new strain every single year produced by the migratory birds specially
ducks .
After millions of losses due to the viral diseases , it is important to fully
understand the virus nature to provide a protective mechanisms and a
prober ways to either treat it or at least stop its spread .
This book handles the diseases of poultry and rabbits in a brief way to
give the veterinary students a good overall view about the diseases , it
is a perfect start for any beginner .
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Virus is a small infectious agent that replicates only inside

the living cells of an organism.
It consists of 4 parts :
1-nuclic acid ( Genome ) . 2- capsid ( protein sheath) .
3- surface proteins. 4- envelope .
there are many classification of viruses but the most used in poultry
are :
1- accordind the type of the nuclic acid :
 single stranded DNA viruses :
- circoviridea ( chicken infectious animia virus ) .
 douple stranded DNA viruses :
- poxviridea ( Avian pox virus ) .
- Herpeviridea ( infectious laryngotrachitis ILT , Merek’s virus ) .
- Reoviridea ( reovirus or viral artheritis ) .
- Adenoviridea ( inclusion body hepatitis IBH , egg drop syndrome EDS , turkey
hemorrhagic enteritis THE ) .
 Single stranded RNA :
- Paramyxoviridea ( Newcastle disease virus NDV , Avian pneumo virus APV ) .
- Orthomyxovirus ( Avian infuanza AI ) .
- Coronaviridea ( infectious bronchitis IB ) .
- Picornaviridea ( Avian encephalomyelitis AE )
 Douple stranded RNA :
- Birnaviridea ( infectious bursal disease virus IBDV or Gumporo ).
2- According the envelope :
 Enveloped viruses : the enveloped viruses multiply much faster and preserve the host
cells much longer , as well as their release from the cell is performed by the ( Budding )
which means that the envelope is a part of the infected host cell membrane .
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- Enveloped viruses in poultry includes : AI , NDV , APV and IBV .

- Envelope viruses easy to disinfect in poultry farms , they are affected mostly by all
types of disinfectants and even killed by the detergents as their envelope in lipid
bilayer .
 Non enveloped viruses : they lacks the envelope as their release from the infected host
cell performed by the cell lyses mostly .
- They includes Pox , Marek’s , AE , Reo , Adenoviridea , IBDV ,CAV and ILT .
- Very hard to disinfect as the capsid is protein in nature , protein is very difficult to
denaturant so specific disinfection only used as Glutaraldehyde and NaOH .
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In the practical study of any virus , there are 11 topic to study , each one will help in the final
identification diagnosis and prevention of the virus , it also will help in the treatment plane ( the
virus has no Treatment but the medication in considered a conservative therapy to prevent the
mortality until the bird immunity stops the virus ).
In each virus there are main points will be:

1-The virus definition :
Consist of 3 parts ( acute , chronic or contagious )( species affected and age )(criteria ).
2-Epidemiology:
a- Etiology:
- Family and genus of the virus .
- DS or single stranded RNA or DNA .
- Cross immunity between serotypes .
- Enveloped or not .
- Zoonotic or not.
- Latency ability or the virus carriers .
- Special proteins responsible for serological and virulence difference .
- Classification if present .
b- Distribution :
- All are world wide .
c- Natural hosts .
d- Lab Host :
-natural host and embryo of the host origin as ECE.
- cell line of the host origin.
e- chemical and physical resistance :
- enveloped viruses can destroyed by environmental conditions as sun light or humidity

as well as all ordinary disinfectant as the envelope is lipid bilayer easily destructed by
lipid solvents and other disinfectant ( QACs – halogens- Formaldehydes )
- non enveloped viruses highly resistant to environmental condition , affected by specific
disinfectants only as NaOH , Glutaraldehyde with QACs , and iodine .
e- transmission :
1-direct : from bird to bird :
 vertical : includes true vertical transmission (viruses infect ovaries AE , NDV ,REO
,Adeno ,CAV) or
egg-shell transmission ( viruses infect oviduct :NDV , AI , IB ).
 Horizontal : orofecal , air droplets , mechanical transmission .
All viruses spread horizontally .
 Latent birds : sheds the virus after stress : ILT , CAV, marek’s and adenovirus .
 Carriers : carry the virus with no C.S , carrier recorded in IB,ILT Adeno And AI.
- Some transmitted with migratory fowls as AI , Tumors, ILT and Adeno family.
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 Venereal : from male to female then offspring : CAV .

2-Indirect : by contaminated utensils , human , vehicles , fumets feces or contaminated
farm , birds cage … etc
 Vectors : insects transmit virus mechanically almost in all viruses but clear in IBDV ,
ILT , marek’s , POX .
3- incubation period : time elapsed from infection till clinical signs .
4-Morbidity : % infected birds in the flock .
5-Mortality : % dead bird in the flock .
6- Clinical signs : includes :
 Upper respiratory : sneezing , mucous discharge from eye and nostrils , eye
inflammation , inflammation of nasal and infraorbital sinuses , conjunctivitis .
 Lower respiratory : couphing, gasping , respiratory rales , increase rate of respiration
with lowered depth .
 GIT : diarrhea , undigested food , poor FCR
 Nervous signs : ataxia , muscle incoordination , torticollis .
 General : huddling , ruffled feather , depression , trembling , decrease activity , food
and water consumption and FCR , emaciation .
 Kidney affection : watery white diarrhea .
 Clinical signs classify the virus into :
 Viruses cause skin lesion: POX , Mareks , plus CAV and ectoparasites .
 Viruses cause nervous manifestation : mareks ,AE , NDV ,AI - and APV 2ry .
 Viruses cause GIT disturbance : NDV , AI , REO , THE + coccidia + pox 2ry + helminth.
 Viruses cause immune suppression : IBDV , CAV, mareks , leucosis , vNDV ,HPAI,IBH.
 Viruses causing respiratory manifestation : NDV , AI , APV ,REO ,EDS ,CELO ,IB,ILT
Secondary POX and marek’s .
 Viruses causing kidney manifestation : Tumors , IB ,IBDV, IBH.
7- PM : vary according virus .
8-Diagnosis :
 CS
 PM ( POX definite diagnosis by PM , all the rest viruses are not )
 Sampling : from virus tropism or blood or shedding feces and mucous .
 Isolation : on embryo of spp origin or cell line of Spp origin .
 Identification : any technique as ELISA and PCR ( rPCR and rRT-PCR for SS RNA only)
 Inclusion bodies IB : I/N Adeno and ILT and Marekes I/C : reo and pox .
9-Vaccination and immunity :
 Live vaccine : used to produce cellular immunity .

Viruses have live vaccine only ( CAV , Mereck’s ,LT ,POX ) .
 Inactivated vaccine : used to produce humeral immunity .
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Used usually after priming with live attenuated vaccine and produce humeral immunity
usually after 3 weeks
Last dose giving before laying 3-4 w ( 18 w of age in layers and 18 in breeders ) .
 Viruses have inactivated vaccine only :
- AI : as it has reassortement ability >> mutation .
- EDS and RHDV : need humeral immunity only .
 Recombinant vaccines : usually use merek’s or pox viruses as a vector .
 In Ovo vaccines : as in IBDV.
 Emergency vaccined viruses : NDV , ILT , POX , DVE.
10-Prevention : biosecurity , good management , vaccination .
11-Control : isolation and culling , : biosecurity , good management ,emergency vaccination.
prevention :
1- biosecurity :
 on farm level :
- distance between the farms must be 2-5 Km .
- all in all out system with one species at a time .
- prevent visitors , or any person to enter the farm .
- traffic control by disinfection before entering the farm .
- water source must be free from pathogens ( lakes water usually transmit bacterial disease
and viral disease specially migratory water fowls virus which affect poultry as AI ).
- prevent any wild or feral birds from entering the farm .
- vectors prevention : -as insects transmits gumboro , ILT , Pox.
by insecticides and insect proof windows .
wild animals as rats , dogs and cats .
- hygienic keeping of ration away from birds and insects.
- Dry litter management to prevent coccidiosis .
- Good ventilation and temperature management to prevent respiratory viruses as APV .
- Workers hygiene .
- Prober disinfection programs .
 On susceptible bird level :
- Must be with MDA from disease that infect birds in fist few weeks as REO and CAV , NDV , AI
by vaccination of breeders .
- Screening the mass immunity when receiving the flock to help determine the vaccination
program according half life time of antibodies and the protective levels .
- Vaccination of current flock with suitable vaccine .
- Do not mix vaccinated and unvaccinated birds in latent infecting viruses as ILT and CAV .
- Good nutrition with good management .
 Internationally :screening migratory birds to notify the neighboring countries by existing dis.
- Do not import live birds from endemic areas without testing, specially latent viruses .
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control :
Farm level Area level
Isolation of infected birds . Applied in contagious diseases as AI :
Burial or burning the dead birds . - Short strategy : localized inf for 1st time :
Injection of hyper immune serum ( THE ,  Sterile zone : eradication of all
DHAV ) birds(1km)
Emergency vaccination (ILT,NDV,POX,DVE). Disinfection and let for 3 w .
Supportive TTT :  Control zone ( 2 KM )
- Immune stimulant ( vit E + selenium ) . Kill all birds within , stop birds
- Antibiotics ( for 2ry bacterial infection if movement
needed ) . Disinfection ,
- Receptors blockers ( as lectine blocks HA  Test zone : ( 5 Km )
receptors which used in AI , NDV) If –ve in all 3 areas = successful
- Bronchodilators as mint oil ( mentophen ) . eradication .
In respiratory diseases
- Vit K in hemorrhagic diseases .
- Multivitamins and minerals generally.
- Use disinfectants in drinking water as
iodine or vercon s.
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Chapter 1 :
Avian
immunology
and vaccination
concepts
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Avian immunology and vaccination concepts

The main function of the immune system is protection against any foreign harmful substances, microbial
or non microbial.
•The immune system characterized by:
1- Discriminates self from non-self

2- Works specifically and non specifically
3- Inducible memory
4- Works locally or systemic
It composed from :
1- Cells
2- Tissues
3- Organs
Cells of the immune system :

They are derived from The Stem Cells which are undifferentiated cells present in Bursa of Fabricous .
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leucocytes
phagocytic phamily lymphoid family
mononuclear polymorph
leucocytes nuclear B-lymphocyes T-lymphocytes
macrophages leucocytes
T-cytotoxic (CMIR)
heterophiles eosinophiles basophiles plasma cells T-helper
T-supressor
hyper-sensetivity anti-bodies
parasitic diseases
bacterial diseases histamine (IgG-IgM)
fungi
( IgE)
Tissues of immune system :

1- tonsils : cecal tonsils
2- payer patches in duodenum .
3-junctions between two different continuous epithelium ( as junction between gizzard and
proventriculus )
4-Gut associated lymphoid tissue as in the rectum there are slongitudinal folds of fixed macrophages .
5-Others ( GALT , SALT , MALT , BALT ) .
Organs of immune system :

Primary lymphoid organs :
1- Bursa of Fabricous : produce the steam cells + B-lymphocytes .

Max. growth at 3 weeks and regress completely at 8-12 weeks (acc. The breed ) .
Present dorsally to cloaca .
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2- Thymus : multi-lobed organ present in the neck . ( 14 lobe 7 lobe on each side ) .
Produce T-lymphocytes .( only 1% of T lymphocyte produced underdo Positive selection –
Selection of T- cells with a weak response to self-antigens, which thus become both
immunocompetent and self-tolerant).
secondary lymphoid organs
1- Spleen :
 Red pulp:
-Destruction of aged RBCs.
-RBCs storage
-Hematopoietic in baby chick .
-Innate and adaptive immune response (CD8 T-lymphocytes, MQ, Natural killer cells)
 White pulp:
-Primary follicle: (Contains B- cell dependent) as B-cells, Plasma cells and dendritic
cells.(Adaptive IR)
-PALS (prearteriole lymphatic sheath) (T- cell dependent): as CD4 T- Lymphocytes,
Dendritic cells, B-cells, MQ and Plasma cells.(adaptive IR)
 Marginal zone: innate response, first line of defense and non antigen specific.
2- All lymphoid tissues .
3- harderian gland : a gland found in eye orbit , consist mainly of B-lymphocytes ( 80%) .
Important in eye drop vaccination .
Classification of immunity :
immunity
non spacific spacific
physical
chemical cellular humeral cellular
parriers 14
Non- specific immunity(innate immunity ) :

1- Physical and chemical barriers :
 As skin ( prevent viruses entrance to the body as they are stratified
squamous keratinized cells which are dead cells )
Some microbes can penetrate the skin as pox virus and multiply in it .
 HCL in stomach : can kill the bacteria for some degree .
 Cilia in bronchial tree : the first line of defense in the respiratory
system and the most important defense against Mycoplasma and
E.coli .
Can be affected by ammonia and viruses , some bacterial strains has
cillioitatic effect .
 Body fluids : contain lysosomes , IgG , IgA , non-specific immune cells.
 Others .
2- Non specific cellular immunity :
 Macrophages , heterophiles , basophiles , eosinophils .
 Most of them are APC ( antigen presenting cells ) .
The role of the non- specific immunity in the production

of the specific immunity :
1- If the physical and chemical barriers can inactivate or kill the antigen , there
is no need for a cellular immunity .
2- If the antigen penetrate the barriers , the non-specific cellular cells as
macrophages start to attack the foreign antigen by theory of self and
non-self :
Macrophages can identify the body cells by some proteins present on the
surface of the cells which called Major-histocompatibility proteins (MHC ) .
Any thing do not carry those proteins get attacked by the non-specific
cellular immunity .
3- After the destruction of the antigen by macrophages , they expose the
effective part of the antigen on their surface and give them to T-helper cells
which will continue the immune response .
( Antigen inactivation and presentation needs at least 3-4 days )
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Specific immunity :
It is composed of both humeral and cellular immunity , after the infection and
antigen presentation , both of them activated by the action of T-helper
lymphocyte as it transform the presented antigen protein into a specific message
to both to T and B lymphocytes allowing the identification of the antigen to them
and initiation of specific immune response as the following :
1- B- lymphocyte : multiply to plasma cells which produce anti-bodies specific
to the antigen presented by the macrophage (needs 3 days) and produce
IgM in the first exposure .( total 7 days )
a part of these multiplication produce memory cells which readily identify
the antigen in the second exposure and multiply to plasma cells and new
memory cells , the plasma cells produce IgG in the second and the following
exposures ( the specific immune response took only 3 days in 2nd exposure).
The antibodies produced also on the mucosal level as IgA but they are
produced faster than the circulating IgG and IgM .
The antibodies is the main component of the humeral immunity .
Antibodies cannot enter the cells , and some antibodies of some microbes
not protective to the other serotypes of the same microbe .
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2- T-lymphocytes : the main cell is T-cytotoxic cell which can identify the
bacteria and also virus-infected cells and kill the cell together with the virus
(kiss of death ).
1) T-cell identify the 2) secrete the lysis 3) the infected cell

infected cell . enzyme . destroyed with the
pathogen inside .
interferons :
They are proteins formed by the cells infected by a virus and affect another
non-infected cell causing stoppage of protein synthesis and thus virus infection
and multiplication in those cells .
Note : blockage theory : some viruses prevent the other viruses even the different
serotypes of the same virus from entering the cell as NDV .
 Immunosuppressive drugs : Tetracycline and florphenicol
 Immunosuppressive viruses in broilers : IBDV , IBH , CIA .
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Vaccination concepts :
vaccine is Injection of a live or killed microbe in order to stimulate the immune system against
the microbe or The administration of an antigen to the body for sensitization of the immune
system against such antigen to produce immune response either cell-mediated or a specific
antibodies .
vaccination aims to produce suitable type of immunity against the virus in the susceptible age
of the virus infection , which can be illustrated to :
1- To prevent:
 Clinical disease and mortality (AI, ND, IB,IBD).

 Loss of body weight (Reo, MG).
 Leg problems (Reo, SA).
 Drop in egg production (ND, IB, EDS).
 Decrease in hatchability (AE, MG).
 Egg transmission (AE, CA, MG).
 Immunosuppression (IBD, CA, MD).
2. To control: An outbreak (emergency) to stop mortality and prevent spread of infection. (in early
stages) as ND, ILT, FP.
3. To provide: Maternal immunity to progeny as ND, IB, IBD, Reo, CA, AE…
vaccination of a bird is done in 3 stages :
1- passive immunity :
The breeders drop immunoglobulins in the yolk which called maternally derived
antibodies (MDA ) , they are IgG type which help in the prevention of the systemic
infection .
This type of immunity is very important in the protection of some viruses , some times it
is the only protection method as in case of :
 AE where MDA protect up to 4-6 weeks and the age of resistance is
approximately 3 weeks .
 REO where MDA protect up to 10 days and the infection occur in the first
2 weeks only ( small margin of the infection ) .
 CIA . MDA protect up to 10 days and the infection occur in the first 2
weeks only ( small margin of the infection ) .
MDA also occur for almost all the other viruses that infect or been vaccinated to the breeder ,
those viruses Ab are either :
1- protective for certain time as :
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 ILT : 10-15 and IP is up to15 days so it is rarely seen in commercial white broilers
( 35 days old ) .
 IBDV : 11-13 days and the infection can occur any time till 8 weeks where the
bursa regress .
2- humeral protective but locally non-protective ( infection occur in the respiratory system level
where the IgG has no protective action ) where the infection occur but its effect is reduced
systemically for a certain period .
 As AI , NDV and IB . ( MDA protection is only 5-7 days ) .

To overcome this problem spray vaccination at day 1 or recombinant vaccines have been used .
( look vaccine types ) .
A number of factors should be considered in determining the best age to vaccinate:
 the initial quantity of MDA .

 rate of maternal antibody decline (t ½ or half life time ) .
 flock maternal antibody levels uniformity.
 pathogenicity level of the field challenge.
 method of vaccine administration.
 type of vaccine to be used.
may be protective, but they may also interfere with the development of active immunity. This
interference makes it difficult to determine the proper timing of vaccination in young birds.
2- early active protective immunity :

Usually , most viruses vaccines are live attenuated vaccines ( look vaccine types )
the aim of these vaccines is to produce memory cells and considered the first virus exposure to
the body , so when the body get the second vaccine or get infected , the immune response will
be stronger and faster ( look specific immunity ) .
this concept called ( priming ) which means application of preparatory relatively weak vaccine
usually live attenuated to give a stronger vaccine later , usually inactivated vaccine for
production of Antibodies .
3-late active protective immunity :

Usually inactivated vaccines , repeated 2 or 3 times the last is before the egg production by
3-4 weeks .
No vaccination is taken during the egg production except for some viruses as NDV and EDS .
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Vaccine types :
1- live vaccine :
 Produce cellular immunity for viruses that require only cellular immunity as
ILT , Marek’s , POX and CAV . (also produce humeral immunity but weak ) .
 Produce local immunity in the first days of the baby chick life , this concept is used
in case of IB , NDV by using it as spray .
 Production of memory cells mainly and with less extend Ab .
 Used in emergency vaccination in case of ILT , NDV and POX .
 The vaccine immune reaction starts within 3-7 days .
 Can be taken orally , eye drops , spray and injection ( merek’s ) .
 Disadvantages : may cause the disease as it may gain pathogenicity in free areas.
Short duration of immunity 15-21 days and may extend to 1 month.
Types :
 Naturally weak as lentogenic strain of ND.

 Attenuated as H120 of IB .
 Athogenic strains as serotype 2 of MD.
 Pathogenic strain of the disease organism as AE in adult birds.
2- inactivated vaccines with oil emulsion or Al OH adjuvant:
 Produce humeral immunity ( Ab) only but which may extend to 9 months and 1
year in some diseases as Newcastle disease,
 Viruses has inactivated vaccine only : AI and EDS .
 The vaccine immune reaction starts within 21 days( stationary phase is more
longer than in living vaccine) .
 Taken only by injection ( stressful ) .
 can be used safely in free areas .
 may cause local or general reaction.
3- recombinant vaccine : use a large sized virus as mareks and POX , their genome is relatively
large ,The idea is to take the gene responsible for the production of the virulace protein of other
viruses ( as HA in AI , HN in NDV , S1 protein in IB ) and put it within their genome , so during their
multiply the virulence protein produced without being harmful to the body ( the original virus
doesn’t exist ) .
 Used in viruses that require long standing immunity and infect the chicken in any
time :
 AI ( vectorimmune )
 IB ,IBDV , NDV.
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Advantages :
 Doesn’t interfere with the virus MDA to be vaccinated .

 No side effects of the original virus vaccine .
 protect against two pathogens.
 High safety level.
 Taken by injection in day 1 old .
 Give two types of immunity.
Disadvantages :
 Not usually available .

 Highly expensive .
 Require susceptibility for both pathogens.
 Presence of maternal immunity of the vector.
4- in-Ovo vaccination : not widely used as the hatcheries in Egypt doesn’t have such a
technology .
Methods of vaccine application :

1- in drinking water :
The easiest and least stressful method , but doesn’t ptoduce even amount of immunity and not
ensure that all the heard has been vaccinated .
Used in almost all the live vaccines .
2- eye drop : give much better immunity comparing to drinking water vaccination due to
presence of harderian gland , but stressful and needs experienced workers .
3- spray : used in most respiratory viruses vaccination , it is easy , but the most important
advantage that this type op immunity gives a very good local respiratory immunity ( IgA ) thus it
is used in IB and NDV vaccines in day 1 baby chick as fine spray ( blockage theory + interferon +
IgA ) and in the later life as coarse spray .
It is also used in ILT and ILT emergency vaccination but as Coarse spray not fine spray .
The usage of any respiratory live attenuated virus vaccine as fine spray in the wrong age will
produce infection specially with ILT and NDV .
4- injection : used in inactivated vaccines and Marek’s vaccines , it is stressful and cause some
times a slight mortality .
5-Wing web.
 Fowl pox vaccines or cholera..

 Vaccinal takes in 95 – 100% of vaccinated birds at 7 – 14 days post vaccination
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emergency vaccination :
therapeutic solution to an infected flock to stop the infection .
 Conditions of emergency vaccines :

- The morbidity is less than 20% .
- No concurrent infection with any other type of microbes .
- Good flock status .
 Viruses can take emergency vaccination : ( have relatively long IP )
- NDV ( about 6 days avr IP , use clone 30 or Avinew strains by eye drops ) .
- ILT ( about 14 days IP , taken by spray or eye drop ) .
- POX virus ( 10 days IP , wing striking ) .
 Emergency vaccine concepts :
1- blockage theory .
2- interferon theory .
Vaccinal Failure :
Factors related to the vaccine :
 Storage (vaccine delivery)

 Mishandling of live vaccines.
 Dose & diluents
 Reconstitution as MD vaccine.
 Inappropriate administration.
 Highly attenuated vaccine .
 Lacking of some serotypes.
Factors related to the bird :
 Age (time of vacc.)

 Maternal immunity.
 Other vaccines (ND , IB).
 General health condition
 Management.
 Immunosuppressives as IBDV ,and mycotoxins .
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Vaccination schedule in broiler flock in general :

1- if the area is highly infected with viruses :
Day Vaccine
1 NDV , IB , IBDV spray or recombinant if the area infected with those viruses or the
production is at annual season of these viruses . ( not necessary but recommended )
7 Hitchner IB . ( NDV+IB ) eye drop .
9 H9 ( AI ) injection ( from Augast till march )
11 H5 (AI ) + NDV injection
12 Gumboro ( intermediate + )
18 LA SOTA or Avinew or clone 30 ( NDV )
22 Gumboro ( intermediate + )
2- if the area is lightly infected and the season in summer or for small numbers under 300
chicks :
Day Vaccine
7 Hitchner IB . ( NDV+IB ) eye drop .
11 H5 (AI ) + NDV injection ( Optional ) .
12 Gumboro ( intermediate )
18 LA SOTA or Avinew or clone 30 ( NDV )
Other strategies according each virus in the viruses chapters .

Vaccination schedule in layer flocks in general :
day vaccine
1 Marecks + IB primer .
3 Provac 3 ( NDV ) inj .
10 H5 (AI )
13 LA SOTA IB
17 Bursen 2 ( IBDV )
30 NDW ( NDV )
40 NDV + IB + AI inj
60 IB primer
75 H9 (AI )
90 POX + AE
109 IB primer + LA SOTA
110 NDV + IB + AI inj
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‫نسخه عرض غير مخصصه للبيع ‪ ...‬حقوق البيع ترجع للكاتب‬
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chapter 2 : Avian parasitic disease
metazoa
external internal
nematod
microscopic cestodes hetrakis
scaly leg syngamus
body mange capillaria
short
ascaridia
Davania
macroscopic
soft tick long
red mites Reliatin
lice
protozoa
enteric hematic
as eimeria spp as plasmodium
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External parasites of poultry :

Lice Tick Red mites -Body mange -Scaly leg
-Depluming -Chronic leg
infestation infestation
mites dermatitis
-Body -Leg mange
dermatitis
definition Permanent Intermittent Intermittent Permanent Permanent
ectoparasite blood sucking ectoparasite
have biting and ectoparasite . attacks only
cutting parts ( at night .
chewing-blood
sucking)
Etiology Menopon Argus persicus Dermanussus Knemidocoptes Knemidocoptes
gallinea and Gallinea Gallinea. Mutans
Live 3 weeks , 1 columbarum. Transmit
one host, one Life cycle 1 M spirochetes
outside host to Transmit zoonotic
lie eggs , on to spirochetes
hatch
Host Chicken , Chicken , Chicken Chicken , Chicken ,
turkey. turkey water turkey and turkey mainly turkey and
fowls , pigeon pigeon caged birds
CS Irritation As lice + Sever irritation Thickened
Restlessness Bird do not Birds pull out shank
Anemia enter the feather Scales become
Drop in egg production nest Area devoid irregular and
from feather loose , raised
with scapes. ruffled in
different
direction
TTT Deltamethrine Deltamethrine Sulphur Deltamethrine Dip shank in
ointment warm water
15% and soap then
apply 10-220%
Sulphur
ointment or
kerosene or
2%phenol
Tetmesol or
nrgavun
Diagnosis :
History , Cs ,
Skin scraping : at lesion rim +10% NaOH then heat , centrifuge , examine ender microscope .
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Disease causing nervous manifestation
1)nematodes
Ascaridia Hetrakis Capillaria Syngamus
Intestinal round Ceaecal worm Hair worm Gap – tracheal
worm worm
species 1-Ascaridia galli Hetrakis galliea Capillaria anulata Syngamus trachea
2-Ascaridia columbi in Domastic birds Crop of chicken and Trachea of
pigeons Hetrakis isolanch turkey chicken and
Chicken – Capillaria columae turkey rarely
pheasant ( obsengata ) fowls
Hetrakis dispar S.I of pigeon -ducks
Fowls
Mode of Ingestion of emberyonated eggs
infection
symptoms General : Violent cough
Growth retardation Extend neck with
Emaciation opened peak
Persistent diarrhea Shaking head .
Low egg production
Paresis in advanced
Death in young as heavy infestation and intestinal obstruction
PM Catarrhal enteritis Typhlitis Cronic catarrhal inf in Presence of y
Excessive mucous Necrosis of affected parts shaped dark red
Adult worm in intestines ceacal mucosa color worm in
Ceacal core in Thickening of mucosa tracheal lumen
heavy of affected parts Catarrhal bloody
infestation. trachitis
Diagnosis : In living birds : egg in droppings by floatation techniques. Y shape dark red
Dead birds : detection of adult of eggs ( direct smears ) from affected worm and D
parts . shape eggs in
trachea and faces
(if swallowed
after cough)
Preventive Avoid humidity : to avoid egg development .
Avoid over crowding..
measures . Avoid contamination of food and water.
Avoid different ages mixing .
Disinfection of houses with 6 % Dekaseptol .
Control earth worm and insects ( mechanical transmission ).
Regular hygienic disposal of dead carcass and droppings .
Infected pens may be rested about 3 months .
Litter management .
Use lime under litter to destroy eggs.
Quarantine measures in newly coming birds‫ز‬
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TTT :
Ascaris :
 Piprazine compounds: affect adult so repeated every 2 weeks .

 Carbon tetrachloride : affect eggs.
 Phenothiazine .
Hitrakis:
 Phenothiazine : alone or with piprazine 4:1 .

 Tetramisol acetate .
Capillaria :
 Phenothiazine.
 Hygromycine
Syngamus :
Individual therapy :
 Tincture iodine 1: 9 in water

 Lugols solutuin 1:5 in glycerin sprayed in nasal opining daily till recovery .
Massive TTT :
 Barium antimony titrate by dusting .

 Methyridine in feed .
Dermanussus
Menopon gallinea Argus persicus
Gallinea
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Knemidocoptes Knemidocoptes
Gallinea. Mutans
Knemidocoptes Knemidocoptes
Gallinea. Gallinea.
Capillaria anulata
Syngamus trachi
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2)Cestodes
Long cestodes Short cestodes .
Raillietina echynopothridea Davania Proglottina
Hymenolepis Spp
Intermediate Arthropods as ants and beetles. Snails and slugs
host
Host Common in pigeons, Common in chicken , turkey , water fowls
.
MOI Ingestion of IMH containing infective stage.
Symptoms General
Constant diarrhea (mucous and blood)
Nervous signs ( heavy infection as they secrete neurotoxin ).
Decrease yellow pigmentation as they interfere with carotene absorption.
PM Very long segmented white worm in Difficult to seen .
intestinal lumen . Catarrhal enteritis
Catarrhal enteritis Velvet like mucosa
Velvet like mucosa
Nodules in serosa as TB and coli
granuloma
diagnosis History :
Detection of worm or egg in dropping lf live birds or intestine in dead birds .
Control Arthropods control by insecticides
Snails control by copper sulphate
Hygienic As nematodes
measures
TTT Kamala
Yomesan
Thiobendazol
Methyrdine
Atebrin
All must be repeated as the explode the segments without head and neck .
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nternal parasitic disease :
Avian coccidiosis
Def : disease caused by different spp of genus Eimeria Chrachtrized by bloody diarrhea , weight
loss and variable mortality and morbidity .
Etiology :
Eimeria spp which are host specific , tissue specific and immune specific .
chicken Eimeria :
name organe pathogenisuty Clinical signs Mort..Morb

E. acervulina Duodenum ++ Bloody brown Moderate mort.
Jejunum diarrhea High morb
E .precox Duodenum + Bloody brown Low mort
E. mitis Duodenum + Bloody brown Low mort
E. nexatrix Jejunum , cecum ++++ ( chicken Bloody diarrhea High mort
killer ) or dropping High morb
E maxima Duodenum ++ Bloody diarrhea Moderate mort.
Jejunum , illume High morb
E-brunetti Illume , rectum +++ Bloody dropping Moderate mort.
High morb
E. tenella Cecum ++++( chicken Bloody dropping High mort
killer ) High morb
Turkey Eimeria Ducks and geese Pigeons

E. adenoids E. truncate ( kidney ) E.lambbeana
E. meligradis E anseris E. columberum
E . meleagrimitis
Epidemiology :
Susceptibility : mostly 3-8 weeks , but can be seen from starting from 10 days .
Distrepution : world wide due to : 1- chort IP ( 4-7 days ) .
2- direct life cycle .
3- resist the environmental conditions and disinfectants .
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Mode of infection : ingestion of large amount ( more than 5000 ) sporulated Oocyst .
Life cycle :
Needs 24-48 hours in approximately 30degree C sporulated Oocyct

Unsporulated and good humidity and oxygen , it remain viabe for
Contain 4 sporocyst
Oocyct 2 days
each one contain 2
sporozoit , it remains
Sporogony viable for years
enzymatic action ( trypsine )

upper intesines due to
the sporocyst wall breaks in the
break down in the gizzard and
The sporulated Oocyct Wall
Mature forming
Zygote
Sporozoit
Infect the intestinal
lining
They bind to form
Shizogony
Gametogony
(asexual division )
Form trophozoit
which undergo
merogony
to form
immature shizont
Male and female Merozoits undergo 2-4 secondary merogony each
one invades new epithelial cells then under go which in turn forms
gametocytes merozoits
sexual division forming
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Coccidiosis : infection by large number of sporulated oocyst , causing clinical manifestation and
macroscopic lesion .
Coccidiasis : infection by small number of sporulated oocyst , insufficient to cause clinical
manifestation and macroscopic lesion .
Sub-clinical coccidiosis : infection by small number of sporulated oocyst , the only clinical sign is
poor food conversion rate .
Pathogenesis : as the coocidia divide and multiply by destroyed the intestinal lining , the cells
stops its functions as digestion and absorption , more over it cause sharp bleeding related to
the depth in which the division occur in the intestinal mucosa , the most pathogenic Eimeria
spp. In chicken are E. tenella and E. nexatris as they reach lamina propria causing massive
hemorrhage and thus high mortality , so they called chicken killer .
Another aspect pf the pathogenesis is when cell necrosis occur with hemorrhage it favors the
clostridia multiplication , so when ever coccidiosis found , the clostridia exist , and both should
be treated together when one of them found .
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clinical signs :
General signs of illness .
Bloody dropping , anemic comp and wattles .
Many infected birds never regain the normal feed conversion rate .
PM : necrosis in the intestinal wall in the Eimeria specific tissue causing hemorrhagic enteritis
as the following :
name organe PM
E. acervulina Duodenum Hemorrhagic enteritis
E .precox Jejunum with distention of the
E. mitis duodenum and jejunum
and visible necrosis
through the serosa
E. nexatrix Jejunum , cecum As E.acervulina in
jejunum
And as E.tenella in
cecum
E maxima Duodenum As E.acervulina but with

Jejunum , illume small focal hemorrhagic
necrosis
E.brunetti Illume , rectum As E.acervulina in the

large intestine but with
fibrinonecrotic enteritis
in chronic cases .
E. tenella Cecum Hemorrhagic typhilitis

( sausage like ceci )
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Diagnosis :
Case history , clinical signs and PM .
Microscopically by detection of unsporulated oocyct in the dropping .
Histopathologically to detect the gametogny ,
Prevention :
1- good litter , ventilation and water lines management .
2- medications as ionophores ( its usage has been declined during the last few years ) , sulpha ,
ambrol or divirdine .
Treatment : compination between sulpha , anbrolium and divirdine .

Diclazuril and toultrazuril .
Vaccination :
Non-attenuated vaccines Attenuated vaccines
Virulent field spp of Eimeria Attenuated spp of Eimeria
Advantages : no need for anticoccidal drugs , Less pathogenic but as immunogenic as the
but if needed , the vaccinal strain re sensitive field ssp . no need for anticoccidal drugs , but
to them unlike the field strains . if needed , the vaccinal strain re sesnsetive to
-no need for multiple types of vaccine spp . them .
-each spp needs a separate vaccine ,
Disadvantages:
-lack if vaccine uniform distripution .
-need apporbriate litter management for the Oocyte circulation .
- short shelf life time .
More expensive than anticoccidial .
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‫‪chapter 3 :‬‬
‫‪diseases‬‬
‫‪causing skin‬‬
‫‪lesion‬‬
‫‪38‬‬
Avian pox virus (APV )

Contagious epitheloma , sorehead , avian diphtheria , canker
Def : contagious disease of all birds (except duck and geese )and all ages chch by nodular formation in
non feathered parts and diphthric membranes on mucous membranes of upper respiratory and
digestive tract .
Epidemiology:
Etiology :
Poxviridae , genus avipox virus (DS DNA , non-enveloped , brick shape )
Strains acc. Pathogenicity :
- Fowl (FPV) - turkey -canary - pigeon pox (PPV)
One serotype so cross immunity present .
Very persistent disease in environment after infection or vaccination .
Transmission :
Horizontal only by :
 Wound and skin abrasion infection .

 Mechanical transmission by insects .
 Airborne .
IP :
 4-10 days in turkey , chicken and pigeon pox .

 4 days in canary pox .
Form CS and PM
Skin form Small gray nodules on unfeather parts of body specially head , vent and wings .
In canary : localized on toes ( foot disease ) .
Wet form In mucous membranes -> diphthiric membranes 1- upper respiratory tract (2ry res . manifestation and
suffocation) 2- Mouth and GIT ( weight loss ) .
In canary : pericarditis or perihepatitis ( same picture of CRD in chicken )
Mixed form Both forms together
Cause 2ry drop in egg production
with mortality up to 50%
Systemic form In canary , high mortality .
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Course of disease about 4 weeks .
Diagnosis :
The only virus that can be confirmed by PM only .
Sampling : skin or diphtheric lesions .

Isolation :
 ECE 10-12 day on cam >> pock lesion.

 CEF or CKC ( avian origin ) >> plaque formation .
Detection and identification :
 EM
 Stain lesion by wright’s ro gimenez stain >> I/C IB (borrel and Bollinger bodies).
 AGPT ,VN , Elisa .
Viral infectivety test : by EID 50
Protection test : ( determine immunogenesity against fowl and pingeon vaccines ) .

Vaccinate 20 SPF chicken , and let other 20 birds un vaccinated , after 3 weeks challenge all
birds with virulent pox virus ,90 % of vaccinated birds should have no lesions , while 90% of
unvaccinated birds have lesions .
Pock lesion on CAM
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Vaccine : live attenuated propagated on ECE or ETE on CAM

: emergency vaccine occure .
spp type Site and method age immunityrevaccine

Chicken FPV Wing web striking 4-8 w 1 year 6 m
1-2m before lay
PPV Wing web striking 4-6 w 3-4 m 2m
Brush anterior aspect of thigh feather 1-2m before lay
turkey FPV Brush anterior aspect of thigh feather 10-12 w 1y 6m
PPV Brush anterior aspect of thigh feather 8w 3-4 m 2m
Canary CPV Wing web striking Weaning age 1y 6-12 m
Vaccine precautions :
 Follow dilution and preservation of the vaccine .
 Prepare vaccine away from the farm .
 Vaccine before 1-2 M of egg production .
 Do not vaccinate birds under stress to avoid post vaccinal reaction .
 Do not mix vaccinated and unvaccinated birds .
 Vaccine vial should opened before immediate use .and used within 2 hours .
 Vaccine should only contact site of vaccine .
 Wash hands after vaccination.
 All vaccine equipment and vials should be incinerated .
 Examine the vaccinated birds after 1-10 days for vaccine Takes :small scapes or swelling
of feather follicles >> if less than 10% the vaccine failed ,
may be due to :
- Inadequate potency of vaccine .
- Improper application.
- Immune birds .
vaccine Takes
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TTT : only in valuable birds :

 Remove diphtheric membranes and touch with tincture iodine :glycrine 1: 4 .
 Antibiotic ( tetracycline ) .
 Appetizers .
In case of outbreak :
 Culling of all affected birds .

 Sanitation and sound management .
 Emergency vaccination of non affected birds.
 Insect control .
Special deferential diagnoses
 Vit A diffeciency. : Easily removed.

 Trichomoniases: :Swap>LM pear shape flagellated protozoa .
 Candidiasis : Detect budding LM.
Notes :
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Marek’s disease ( MDV )
Def :Lympho-proliferative neuropathic disease of chicken , turkey, geese and quell caused by cell
associated oncogenic herpes virus .
Epidemiology :
Etiology : herpes virus ( DS DNA , non enveloped , cell associated virus )
Classification : according serotypes : ( cross immunity present )
1- Serotype one virus = gallid herpes virus 2

 Include all pathogenic strains .
 Has the following pathotypes :
- Mild ( mMDV )
- Virulent ( vMDV )
- Very virulent ( vvMDV )
- Very virulent plus ( vvMDV +)
- New emerging pathotypes.
2- Serotype 2 = gallide herpis virus 3
 Avirulant used in vaccination .
3- Serotype 3 = turkey herpes virus = melligradis herpes virus 1
 Used in vaccination .
 All cell associated in lymphocytes but cell free at feather follicle only.
Spp affected :
Chicken mainly then turkey > infection at 6-24 w > deaths start at 8 w
Transmission :
 direct and indirect transmission by airborne rout as virus sheds from feather follicle and persist
in dust for many months .
 minor way by insects and beetles ( Alphitobius diaperinus ) .
IP :
 3-4 W TILL MANY MONTHS ( latency ) .
 6-7 days in non-lymphoproliferative forms .
Mortality : 25- 60% in layers and breeders non or 0.5% broilers.
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Pathogenesis and replication :
A) Phase 1 = early productive restrictive infection .

T lymphocytes mainly Transient atrophy of
Inhalation of virus and (CD4 and CD8) thymus with I/N IB
IP
replication in non- infect
lymphoid tissue Less extend B 8-14 Transient atrophy of
lymphocytes d bursa with I/N IB
Recovery in 6-7 days Permanent

infection show CS
Phase 2 = latent infection
Presence of virus DNA and absence of virus protein and not
detected by body immunity .
Phase 3 : second phase of cytolytic infection

Cell mediated viremia localize virus in
Visceral
Nerves
organs
Feather
follicle
shedding Focal cell death and inflammation
Phase 4 : development of
lymphoma
By uncontrolled lymphoid cell growth in
visceral organs and nerves
45
Forms cs pm Age Mortality
Neural form Paralysis of peripheral nerves Nerves 3 times Layers : Layers : 0-20%
( classical form ) Paralysis of sciatic nerve ( leg ) normal Occasional
(rang paralysis) Paralysis of vegus nerve ( neck ) size gray in color 8-20 w
Paralysis of brachial plexus cause Loss of striation
respiratory muscles paralysis and
secondary respiratory signs
Dropped wing
Pendulous crop
Eye form Fish eye .. discolored iris ( mononuclear cell infiltration ) Rare in all none
..unilateral or bilateral blindness Layers > 10 w
Skin form Lymphomas ( tumor ) at hair follicles . Layers : rare none

4-8 w
Broiler:
common
Visceral Lymphomas in internal organs Common in 0-60%
Atrophied thymus . layers 4-90 w
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Microscopic lesions :
Thymus : degeneration and atrophy , some times lymphoid infiltration .
Fatty proliferative changes in intima of coronary , mesenteric ,aorta and celiac arteries .
Diagnosis :
Sampling : skin lesions , tumors , buffy coat.
Isolation : ECE >> on CAM >> pock lesion .
DEF or CKC or OU2 >> plaques less than 1 mm .
Viral markers in tissues : viral probes , PCR , Electron microscope , monoclonal Ab.
Detection : FAT , AGPT , VN , enzyme linked immune peroxidase.
DD with Leucosis
feature Marek’s disease Lymphoid leucosis

Age Above 6 weeks Above 16 weeks
Symptoms Skin , ocular and paralysis Non specific
incidence 5 % in vaccinated flocks Rarely above 5 %
Microscopic and macroscopic features
Neural involvement yes no
Liver tumors diffuse focal
Bursa involvement Less ( transient atrophy ) Major ( nodular lesions )
spleen Atrophied or inter follicular tumor inter follicular tumor
Skin muscles and yes no
proventriculus lymphoma
Polymorphic lymphocytes as lymphoblast
lymphoblast , T lymphocytes ,
reticular cells , rarely B lymphocytes .
Neoplastic cells T lymphocytes B lymphocytes
vaccine yes No
Vaccines :
Serotype 1 : as R2/23 only cell associated vaccine. ( alone or combined with 2 and 3 > breeders-layers)
Serotype 2 : SB -1 non pathogenic only cell associated vaccine.( usually with 1 for breeders ) .
Serotype 3 : FC 126 cell associated and cell free vaccine. ( broilers , with 1 and 2 for all in winter) .
So there are monovalent , bivalent , trivalent vaccine.
 Needs 2000- 6000 plaque forming unit per chick .

 Maternal Ab affect the cell associated vaccine.
 Ab needs 7 days too produce .
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 1st day vaccine and revaccined at 12 day . ( only injection as it is cell associated virus )
Other vaccines :
1- Recombinant :
2- Deletion mutant vaccine.
3- Selection of other variant strains.
Notes
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lesion Other Spp Mort, morb Lab
lesions affected
POX Nodular skin lesion on area devoid - Chicken High morb. ECE:pock
of hair and Low or no lesion
Diphthiric membrane on mucous turkey of mortality CEK: plaque
membrane of upper respiratory all ages formation
and
EM
digestive tract.
Mareks Lymphoma in feather follicles . Tumors in Chicken Common in I/N IB
( nervous clinical signs ) visceral and broilers and As pox
organs turkey and rare
and geese in layers
Lice Irritation -
nerves. Chicken , - -
Deferential diagnosis of diseases causes skin lesions :
Restlessness turkey.
infestation Presence of lice on skin
50
Tick Irritation - Chicken , - -

Restlessness turkey
infestation Presence of tick on skin water
fowls ,
Red mites Irritation - Chicken
pigeon - -
Restlessness turkey
Presence of mites on skin and pigeon
Body Area devoid from feather with - Chicken , - Skin scraping
scapes turkey
mange
Scaly leg Thickened shank Scales - Chicken , - Skin scraping
become turkey
irregular and loose , raised and caged
ruffled in birds
different direction
chapter 4 :
diseases
causing
nervous
manifestation
51
Avian encephalomyelitis (AE )

Epidemic tremors
Def : acute viral disease affecting young checks ( 1-3 w up to 6 w ) and turkey ,chch by ataxia , rapid
tremors of head and neck , transient drop in egg production in layers and low hatchability in breeders.
Epidemiology :
Etiology : One of picorna-viridae , SS RNA , non enveloped ,
Classification :
serological similar , with 2 different pathotypes :
 Entero-tropic : transmit vertically or horizontally by orofecal route and cause neurological signs.
 Embryo adapted strains : transmit vertical and by parenteral routes , no horizontal transmission
,cause encephalomyelitis and muscular dystrophy.
transmission IP morb mort CS

Vertical ( in ovo 1-7 days 60% 50% Embryonic death in last 3 days of incubation .
infection ) Lower hatchability 20%
Cause incubator horizontal transmission .
Hatched chicks suffer from CS as following in horizontal :
Horizontal, by >11 days 40% 25% Blindness due to eye opacity .
orofecal route Dull expression of eye .
Ataxia and muscular incordination.
Inclination at hip joint .
Head and neck tremors ( also in layers ) .
Inability to movement >> death .
Layers : transient drop in egg production with no mortality.
PM
1- Opacity and bluish discoloration of lense.
2- Whitish area on gizzard ( infiltration of leukocytes ) .
52
histopathology :
 disseminated non- purulent encephalomyelitis and gangeliolitis .
 mononuclear microgliosis and perivascular proliferation in CNS
 zinker necrosis of muscles + sacro-lemmal proliferation and heterophils infiltration.
 infiltration of leukocytes in eye and gizzard .
Diagnosis:
CS , Age , Histopathology .
 Sampling : brain
 Isolation : ECE I/Y 5-7 days >> hatching >> observe the CS and histopathology in first 10 days .
>> followed by FAT or ELISA .
Chicken cells as CK .
 Detection : indirect FAT , VN , passive HA .
 Embryo- susceptibility test :
-inculate 2 groups of ECE 1- from tested flock 2- control .
- I/Y with 100 EID50 egg adapted virus .
- if 100% of eggs affected >> susceptible flock .
-if < 50% affected >> immunity( protected flock ) .
- evaluation of immunity by ELISA . .
Vaccination and immunity :

MDA : 4-6 w .( if the baby chick has NDA it wont get the infection aa age of resistance 2-3 weeks)
Active immunity : after 11 days of infection .
Age resistance after 2-3 w of age .
Aim of vaccination :
1- Protect young chicks by vaccinating the breeders (MDA ).

2- Protect layers from transient egg production .
Live attenuated vaccine : strain 1143 enterotropic ( not embryo-adapted )
 At more than 8 weeks till 4 weeks before egg production . in drinking water.
Inactivated vaccine :
 14-18 w inj .
TTT : culling of the infected chicks .
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Avian influenza AI :
DEF : highly contagious acute septicemic disease of almost all birds , associated with respiratory ,
nervous ,GITand reproductive symptoms .
Epidemiology :
Etiology
Orthomyxoviridae , enveloped SS RNA virus , enveloped or pleomorphic .
Contain 8 segments of RNA encodes 10 proteins the most important are :
1- Hemagglutinin ( HA ) :
- Used in virus for attachment and fusion into the cell .
- Determine virulence and pathogenicity of the virus
- Determine immune response of the body ( no cross immunity between deferent HA )
- Determine the type of the vaccine .
- identification of the virus
2- Neuraminidase ( NA) :
-virus budding out of the cell.
- prevent virus particles agglutination .
- determine the subtype
-Determine the type of vaccine .
- identification of the virus.
Causes of mutation in AI :
- HA and NA are produced by different segments and the are 18 type of HA and 11 type of NA
any change or replacement in structure of these segments will produce new virus .
- Antigenic drift: multiple mutation ( as it is RNA ) the whole genome replaced every 25 years.
- Antigenic shift ( reassortment ) : exchange the whole segment between 2 AI viruses inside
the host cell .
- The ability of AI of interspecies transmission .
- Concurrent infection with different serotypes of AI occurred . ( specially in pigs ).
Influenza types :
1- Influenza type A : birds , pig , human , horse and marine mammals . ( HPAI-LPAI )
2- Influenza type B : Human , pigs
3- Influenza type C : Human and pigs .
Zoonotic importance :
- AI is zoonotic disease , human is dead end host .( no human to human transmission ) .

- AI though to be infect the human by modification in the pigs which have both Human and -
birds receptors in the respiratory system .
- Only H5N1 is zoonotic .
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Birds susceptible :
- All birds at any age .

- duck only affected by H5N1( sudden death ) but carry the other serotypes .
- pigeon resists the CS but carry the infection .
transmission :
1- no vertical transmission but the virus sheds on the egg shell in infected birds.
2- Horizontal :
- Airborne .
- Orofecal .
- Drinking water ( by the ducks droppings in the lacks(34) during the migration ).
- Contaminated fomites .
3- Carriers ( fowls and pigeon ) ( recovered birds sheds virus for long time ).
IP : 3-4 days .
Chicken and morb mort CS PM

turkey
LPAI 100% 5% Respiratory complicating virus . Upper and lower respiratory inflammation.
Sharp Decrease in egg quality Ovary regression with inflamed ova and
and quantity . salpengitis >> egg peritonitis.
Mild respiratory symptoms and Nephritis .
may be asymptomatic Fibrinous enteritis in turkey
Diarrhea Firm hemorrhagic pancreas.
HPAI 100% 50- Sudden death . Cyanosis. With facial Edema .
100% Cyanosis. With facial Edema . Swollen head , neck, and legs.
Hemorrhages on shank . Petechial hemorrhages on the muscles, serosal
Torticollis surfaces specially epicardium , mucosa of
Greenish diarrhea . proventriculus and gizzard .
+ as LPAI with less respiratory . Enteritis with lymphoid regression ,
Necrotic foci in heart and parynchymatous
organs .
Pneumonia .
Atrophied bursa and thymus .
+ as LPAI .
Wild birds
LPAI - - No clinical signs -
HPAI - 10-20% Sudden death only . Respiratory inflammation and encephalitis .

H5N1 : diarrhea and nervous Septicemia in ducklings + encephalitis .
manifestation ,specially in
ducklings.
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Ostrich
LPAI 100% 5% As poultry ( in young ) . Pneumonia + air sacalitis + septicemia +
congestion of internal organs .
HPAI 100% 30% Nervous manifestation . Head , neck , leg edema + hem. Enteritis .
Mouth breathing . Enlarged pancreas and spleen + as LPAI
57
Diagnosis :
CH- CS – PM
Sampling :
1- take parynchymatous organs or tracheal &pharyngeal swaps or at least 1 gm of fresh dropping

2- put in PBS at 7-7.4 pH with Antibiotic and antifungal .
3- stored at 4 C for 4 days Max.
isolation :
 on SPF or SAN / on alantoic sac >>> death within 24 H with hemorrhages and HA .
identification :
 AGPT
 HA and HAI ( exclude EDS . NDV and other paramyxoviruses , if –ve for AI > continue AI
 NA profile .
 RT- PCR ( most used ) .
Immunity :
Depend on humeral immunity on systemic and mucosal levels .
Maternal immunity : 2 weeks .
Vaccines :
No live attenuated ( due to the reassortment ability of AI ) .
1- Inactivated vaccines with full genome : ( only local – autogenous – types )

- LPAI ( H9 ) >> aims to lower CS and mortality .
- HPAI ( H5 ) >> aims to lower the shedding.
- homologues ( one HA one NA as H5N1 , H9N2 …etc )
- Heterologous ( one HA varying NA )
 If Ab for any unvaccinated HA or NA found >> infection .
 Always leave 25 birds unvaccinated as a monitor for the herd .
 Commercially found alone or with NDV and / or IB .
 Used in broilers at day 11 and revaccinated in layers once or twice ( before 3-4 w of egg
production )
2- Recombinant vaccines :
On hichner or lasota or Marek’s .
3- In ovo vaccine .
TTT :
Immunestimulants containing sialic acid receptors inhibitors as lectin ( superimmune or
immunare ) and TTT of secondary infections .
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NEWCASTLE DISEASE (ND)

Def :acute or subacute contagious septicemic disease of domestic and wild birds characterized by
respiratory symptoms, nervous manifestations and high losses in susceptible birds ,It change in egg
quantity and quality in adult birds.
Epidemiology:
Etiology :
Group of closely related viruses, which form the avian paramyoxvirus type 1 (PMV-1) Genus Avula virus
one serotype with minor differences between the strains by VN .
SS RNA ,enveloped, HA,pleomorphic , six genes forming seven proteins , most important are :
1- HN
 hemagglutinin activity : agglutinate red blood cells (RBCs) >> used in diagnosis by HAI
 Neuraminidase Activity : gradual elution of agglutinated RBCs and prevents the
reattachment of released virus particles and virus clumping.
2- F, fusion protein :
 Fusion of the viral and cell membranes so nucleocapsid complex enters the cell.
 synthesized as a nonfunctional precursor , requires cleavage to FI and F2 by host proteases.
 Affect pathogenicity .
Avian paramyoxviruses include nine serotypes (PMV-1to PMV-9) with some serological relationship .
Five pathotypes :
 Velogenic viscrotropic (vvNDV ) = Doyle’s form =Asiatic or exotic

- highly virulent and lethal for all ages for chickens, less in turkey .
- hemorrhagic lesion in the digestive tract.
 neurotropic velogenic (nNDV ) =Beach’s form .
- NVND)– Acute and fatal in chickens of any age.
- causing neurological and some respiratory signs.
 Mesogenic = beaudette’s form :
- Mortality and nervous signs in young.
- used as vaccines in previously immunized birds. ( Komarov)
 Lentogenic = hitchner’s form
- Mild subclinical Can affect any age.
- Used in vaccines
 Asymptomatic (used in vaccines ) .
- gut infection with no obvious disease .
- used in live vaccines .
Measure pathogenicity : see diagnosis
Zoonotic cause conjunctivitis
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Ninteen Genotypes included with in :
 Class 1 : nine Genotype ( IX ) Avirulent

 Class II; 18 Genotypes (I-XVIII) .
- Genotype II (vaccinal strains which are La sota and B1 )
- Genotype IV Virulent (VND)
- Genotype VII vVirulent (vVND)
Natural host : ( 241 species are susceptible)
Chicken , then turkey severely affected specially the youngs .
Duck and geese few or no clinical signs . young ostrich nervous signs , pigeons diarrhea nervous signs.
Transmission :
 Egg shell transmission . with less extend true Vertical transmission .

 Horizontal transmission directly and indiredtly by orofecal ( ingestion) route and air droplets.
 virus survives for long periods at ambient temperature, especially in feces for 7 d – months .
 flying birds and insects
IP : 2-15 D ( Days average ) .

Clinical signes :
pathotype Broilers Layers
vNDV -Sudden death in day old chick . -(drastic drop )in egg production within 24 to
-General + respiratory + septicemia 48 hours followed by high death losses
-edema around the eyes and head. ( 10-15 % in 24hours) stop in 7-10 d.
-Greenish diarrhea -Survived birds may have permanent
-Nervous manifestation . neurological signs and permanent destruction
-Mortality : 100% in unvaccinated birds . of reproductive tract so egg production never
Immunosuppression return to previous levels.
-Abnormal egg quality .
-Mortality : 100% in unvaccinated birds .
NVND -Sudden onset of severe respiratory drastic drop in egg production.
disease followed a day or two later by 50%
neurologic signs.
Mortality : 90%
MESOGENIC Respiratory and nervous signs marked drop in egg production that may last
for several weeks.
LENTOGENIC -respiratory disease Non ( used in layers and breeders vaccine
-mortality more by La Sota strains during the egg production )
complicated by infections with other
micro-organisms.
-Vaccination or infection of broilers close
to slaughter with these viruses can lead
to colisepticemia or airsacculitis with
resulting condemnation.
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PM
1- Hemorrhages in : ( GIT )
 Tips of provectriculus glands .
 Bottom shape Hemorrhagic ulcers in duodenum ( necrosis of payer patches or intestinal wall ).
 Cecal tonsils .
 Rectum : zebra marking Hemorrhages .
2- Respiratory tract :
 Air saccalitis .
 Trachitis.
 Hemorrhagic conjunctivitis .
 Pneumonia.
3- Encephalitis .
4- Focal necrosis of the spleen. ( vNDV )
5- Layers
 Salpengitis and follicular atresia and ovarian follicles are often flaccid and degenerative.
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Diagnosis
Sampling : Trachea and intestine , should always include feces, intestinal contents or cloacal swabs.
Add antibiotic and antifungal then
( isolation ) inculate ECE I/alantoic , 9-11 day , daily candling till embryo death
To take alantoic fliud and apply HA test on chicken RBcs then HAI .
Cell culture : Plaque formation in chick embryo cells is restricted to velogenic and mesogenic
Cytopathic effects the formation of syncytia with subsequent cell death .
Detection : PCR – ELISA - Sequence technology - Pathogenicity test .
Pathogenicity test : lentogenic Mesogenic Velogenic

hours between infection and death of 10 day-old embryos
Mean death time > 90 60,90 50-60
hours between infection and death of 10 day-old embryos
Intracerebral Path. Index < 0.5 1.0-1.5 > 1.5
1-day old chicken
Intravenous Path. Index 0,0 0.0-1.0 > 2.0
6-8 weeks old SPF chicks
Vaccines :
 Live lentogenic : LaSota, clones of LaSota, Hichniter B1, F. ( day 7- 18-20 ) or any age even
during the egg production .
 Inactivated lentohenic vaccines : day 12 , and revaccinated 4-6 w before egg production(any
age)
 Live attenuated mesogenic as komarov ( after 1 mounth in previously vaccinated birds ) .
 Recombinant usually on THV on F protein or other vectors .
TTT :
1- emergency vaccination ( look vaccination chapter ) .
2- Immune stimulants containing sialic acid receptors inhibitors as lectin ( superimmune or
immunare ) and TTT of secondary infections .
3- TTT of 2ry infection and the vital organs .

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‫‪64‬‬
CS lesion Mort, Special lab
cestodes General Presence of worm in morb
low Floatation
Constant diarrhea the lumen of technique
Defferential diagnosis of diseases causing nervous manifestation
Nervous signs intestines . for detection of

Decrease yellow eggs
pigmentation
nematodes Growth retardation Presence of worm in low Floatation
Persistent diarrhea the lumen of technique
Low egg production intestines . for detection of
Paresis eggs
Death in young
AE Blindness due to eye Eye Opacity -Whitish Morb : 40-60% rRT-PCR
opacity area on gizzard Mort : 25-50%
Ataxia and muscular
incordination
Inclination at hip joint
65
Head and neck tremors
AI Sudden death – green Hemorrhagic syndrome Morb: 100% rRT-PCR

diarrhea –respiratory Respiratory and genital Mort : 5-100% HA-HI
manifestation - system inflammation
Cyanosis Thymus,bursa atrophy
NDV Sudden death – green Hemorrhages Morb :100% rRT-PCR
diarrhea –respiratory -Tips of provectriculus glands Mort : 0-100% HA-HI
manifestation -Buttom shape
Hemorrhages in duodenum
-Cecal tonsils
Rectum : zebra marking
Mareks Paralysis of sciatic nerve ( leg ) Lymphoma in feather Common in layers I/C IB
Paralysis of vegus nerve ( neck ) follicles . ECE:pock lesion
Paralysis of brachial plexus cause Tumors . CEK: plaque
respiratory muscles paralysis and formation
secondary respiratory signs EM
Dropped wing
Pendulous crop
‫‪chapter 5‬‬
‫‪diseases‬‬
‫‪causing GIT‬‬
‫‪disturbance‬‬
‫‪66‬‬
Reovirus ( respiratory enteric orphan )

Viral arthritis
Tenosynovitis
Def : acute and chronic disease of chicken caused by different serotypes and pathotypes of avian
reovirus , chch by arthritis and swollen and hotness hock and tarsotibial joints and rupture of
gastrocnemius tendon .
Epidemiology:
Cause
different serotypes and pathotypes of avian reovirus . ( nonenveloded Ds RNA )
classification :
1- According to size : small – medium – large .
2- According pathogenisity : 5 serotypes .
Transmission :
1- Horizontal : orofecal and respiratory infection. ( less than 2 weeks ) .
2- Vertically .
Age resistance start at 2 weeks .
IP : vary according the pathotype and M.O.T.

CS PM
Lameness Bilateral Gastrocnemius , digital flexors swelling and rupture .

( arthritis ) Inflammation and edema of tendon sheath .
Acute inflammation contain straw color or bloody exudate . ( lameness )
Most important in male roster bird 12-16 w ( cannot stand to fertilize the hens )
Chronic hardening and fusion of tendon sheath , erosions in the articular cartilage and
underlining bones .
Runting-stunting Enlarged proventreculus – small gizzard – pancreatic atrophy – orange mucous in intestinal
syndrome( Mal- lumen – helicopter syndrome.
absorbtion The result secondary are >> encephalomalacia rickets – bursa and thymus atrophy
syndr.
Respiratory Serous inflammation of the respiratory tract ( self limiting unless combined with other
manifestation. respiratory diseases )
67
Diagnosis :
Isolation >> intra yolk or on CAM >> death within 3-5 days with S/C hemorrhage 7-8 days PI
May also have dwarfing and enlarged spleen and liver with necrotic foci .
>> chicken kidney cells >> intracytoplasmic eosinophilic and basophilic inclusions.
Detection : RT-PCR – ELISA – virus neutralization test .
Vaccine : for breeders and layers

By strain S1133 : live attenuated > day 11-12 S/C
Inactivated > 18 W
In ovo > experimental .
Disinfection : 0.5 % organic iodine + vaccination as it depend mainly on maternal immunity .
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‫‪69‬‬
Adenovirus infections ( AVI )

:
Def : group of infections affect mainly poultry chch by enteric , hepatitis ,splenomegaly ,
hydropericardium ,Anemia , decrease egg production , and immunosuppression .
NOTE : can act as Co-infectors or help other viruses as it gives replicating gene to defected ALV .
Epidemiology :
Etiology :
 adenovirus non enveloped DS DNA virus .

 Replicate in nucleus and give basophilic or eosinophilic inclusions bodies .
 Hexon is the mjor protein producing specific immunity .
Classification:
1- Group I adenovirus: ( genus adenovirus ) :

 inclusion body hepatitis.
 Quail bronchitis ( CELO virus = chicken embryo lethal orphan= mild respiratory infection ).
 Fowl adenovirus ( 12 serotypes – 5 spp )
 Hydropericardium syndrome = Angora disease ( high attitude birds ) .
2- Group II adenovirus: ( genus siadenovirus )
 Turkey hemorrhagic enteritis .
3- Group III adenovirus: ( genus Atadenovirus )
 Egg drop syndrome .
General CHCH of adenoviruses :

 Non HA except - CELO and EDS >> rat and human O type .
-EDS >> chicken RBCs .
* cultures : must be from Spp origin.
* ECE : embryo of Spp origin >> curling and dwarfing .
IN inclusion bodies in site of infection .
HI + serology .
Transmission :
 Vertical .
 Horizontal ( mainly orofecal + trachea and kidney )
 Shedding in 2 waves : 4-6 and 15 weeks in layers under stress of sex hormones > latency .
70
Turkey hemorrhagic enteritis : ( THE )

def : acute infection of young well fleshed turkey ( and chicken ) 6-12 w chch by sudden onset and short
course high mortality( 60% in 10 days ) , bloody droppings and immunosuppression .
PM :
 Well fleshed bird

 Anemia + hemorrhages on Ms heart, liver , proventriculus .
 Hemorrhagic enteritis .
 Spleen : marbled in live birds , small in dead birds.
TTT :
 Inject 0.5 ML immune serum .

 VIT K
 Antibiotic
 Electrolytes.
71
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‫‪72‬‬
dis CS lesion Morb. spp Special lab
Bloody diarrhea Necrosis of intestinal wall
Mort
vary Chicken . Fecal smear to reveal
coccidiosis
(necrotic focci) turkey, duck unsporulated oocyst
Sosage like ceci (E tenella) and geese
Deferential diagnosis of Diseases causing GIT disturbance
>3 w
Reo virus Runting stunting syn. Atrophied pancreas 1-3 w I/C IB
Helicopter syndrome Ruptured ligaments , RT-PCR
arthritis
THE bloody dropings and -Well fleshed bird Mort.60% Turkey and I/N IB
immunosuppression Anemia + chicken PCR
-hemorrhages on Ms heart, 6-12 w
liver , proventriculus .
-Hemorrhagic enteritis .
-Spleen : marbled
NDV Sudden death – green Hemorrhages Morb Chicken , turkey HA >> HI
diarrhea –respiratory -Tips of provectriculus glands :100% rRT-PCR
73
manifestation -Buttom shape Hemorrhages in Mort : 0-
Nervous manifestation duodenum 100%

-Cecal tonsils
-Rectum : zebra marking
Hemorrhages
AI Sudden death – green Hemorrhagic syndrome Morb: Chicken , turkey HA >> HI +
diarrhea –respiratory Respiratory and genital system 100% All spp rRT-PCR
manifestation – inflammation Mort : 5-
Cyanosis Thymus,bursa atrophy . 100%
Nervous manifestation
Wet pox Diphthiric membrane High morb. Chicken and I/C IB
on mucous membrane Low or no turkey of ECE:pock lesion
of upper mortality all ages CEK: plaque
digestive tract. formation
EM
Chapter 6 :
Diseases
causing
immune-suppression
and
hemorrhagic syndrome
74
All these viruses cause hemorrhages on shank, pectoral muscles and junction between proventriculus
and gizzard ( hemorrhagic syndrome )
Inclusion body hepatitis : ( IBH )

Def : dis of young chicks 3-7 w chch by sharp increase in mortality , aplastic anemia , splenomegaly ,
hepatitis , immunosuppression ( both bursa and thymus affected ) .
mortality 30% reach peak in 3-4 days and stops 5 d – 3 w .
CS : As CAV
PM :
Pale comb and wattle . - liver : enlarged , pale hemorrhagic and friable .
Kidney : enlarged + hemorrhagic . - bone marrow : watery and bale
Atrophied bursa and thymus. - hemorrhagic syndrome .
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Infectious bursal disease virus (IBDV)

Gumboro
Def : acute highly contagious viral infection of young chicken chch by perfuse watery diarrhea ,
immune suppression and variable mortality .
Epidemiology :
Etiology :
Birnaviridae virus , double stranded RNA with A and B segments , segment A produce VP2 which
responsible for immune response and antigenic variation .
Non enveloped virus .
Classification :
1- Serotype 1 = pathogenic :
 Classical .
 Variant ( not affected by classical Ab ) ( its Ab protect against classical strains infection)
 vvIBDV ( similar to classical Antigenically ) .
2- serotype 2 = non-pathogenic ( 30% relationship with pathogenic ) .
transmission :
only horizontal as :
- orofecal and respiratory route .

- insects transmit the virus mechanically .
- very persistent virus remain viable for about 122 days .
- shedding start day before CS .
IP : 2-3 days .
Morbidity : 100%
Mortality : 1-70 % according secondary infection
Factors affecting mortality :
- age : 3-5 w ( the max growth of bursa the virus tropism )

- maternal immunity : last for 2-3 w acc. Breeder age and vaccines .
- viral virulence : vvIBDV > variant > classical > serotype 2 .
- hygienic measures : disinfection by iodine or formalin .
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Clinical signs :
- sudden onset .
- perfuse watery diarrhea .
- picking of vent .
- General CS .
PM :
- Bursa : edematous in first 3rd
Hemorrhagic in 2nd third . ( sac of blood )
Atrophied in last third .
- Enlarged spleen and liver with necrotic focci on spleen .
- Nephrosis and dehydration .
- Hemorrhages on thigh , pectoral Ms and junction between proventriculus and gizzard .
Which called hemorrhagic syndrome( look page 38+)
- Variable PM acc 2ry infection .
Mortality curve : ( ‫ )مهم جداااااا الن الجمبورو ممكن يتعرف من الكيرف بتاعه بس‬:
Mortality curve
100%
90%
80%
70%
60%
50%
40%
30%
20%
10%
0%
DAY 1 DAY 2 DAY 3 DAY 4 DAY 5 DAY 6 DAY 7 DAY 8 DAY 9 DAY 10 DAY 11 DAY 12
1-3: IP ( course of disease 9 days )
Day 2: start shedding .
3-6: first third of mortality ( sudden start of mortality and CS ) .( edematous bursa )
6-9: second third of mortality (peak of mortality + hemorrhagic bursa )
9 – 12: last third of mortality: (regression of mortality + clinical signs + mortality reached 30-70% )
(atrophied bursa) .
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Subclinical Gumboro :
Infection occur in first week , thus no development of bursa nor humeral immunity , with No CS or PM
for Gumboro except atrophied bursa , the only observed problem is immune suppression with multiple
unrelated diseases with vaccinal failure .
Vaccination :
Live attenuated vaccine :
Classified as : mild – mild plus – intermediate – intermediate plus – Hot .
Variant strain protect against both variant and classical strains .
10-12 d , 20-24 d, 10-14 w
Give protection for 1-3 weeks .
Inactivated vaccines :
16 – 18 w >> protection for 4-5 w .
In ovo vaccine .
Diagnosis :
Sampling : bursa or spleen .
Isolation : chicken embryo bursal or kidney cells . >> plaque under agar .
Identification : Ab catch ( indirect serology ) not useful as maternal Ab may interfere .
Use Elisa and RT- PCR .
TTT :
- E sel .
- Vit K .
- Antibiotic .
- Renal wash.
- Increase T by 2 degree.
- Disinfection by iodine.
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‫‪79‬‬
Chicken infectious anemia (CAV = CIA )
Def : acute viral disease affect chicken from 2-4 w chch by anemia , low hematocrit value stunting
growth atrophy of lymphoid organs and immune suppression .
Epidemiology :
Cause :
Gyro virus family circoviridae ( SS DNA non enveloped ) .
One serotype , with 3 proteins VP1 – VP2 (needs to vaccines ) and VP3 .
Spp affected : chicken only . 2-4w.
Transmission :
 Vertical .
 Horizontal : direct and indirect to :
- Hens >> if –ve Ab >> shedding >> after production of Ab > no shedding till half life time of
the Ab >> start shedding again ( latency ) .
- Baby chicken and develop CS if infection in first 2-3 w . if after 2 w only immunosuppression
and low FCR
 Venereal: from the male roster to the hens> no CS on Hens > vertical transmission to eggs .
IP : 2 w > CS 2 w > one week after CS mortality stops >> 3 weeks after end of CS start Ab production .
Shedding : start one week post infection ( one week before appearance of CS ) .
So , there are 2 peek of mortality , the first at 14 -16 days , second week after ( 21-22 day ) .
Morbidity : more if vertical transmission occur

Mortality : 10-30% , up to 60% if mixed infection occur .
CS : general + anemic comp, wattle , eye lids and legs + petechiation and ecchymosis .
PM :
1- Pale gelatinous bone marrow.
2- Atrophied thymus + ( transient atrophied bursa )
3- Blue wing disease .
4- Hemorrhagic syndrome.
80
Diagnosis :
CS – CH – PM
Low hematocrit value ( 6-27% ).
Sampling from blood or buffy coat .
 Isolation :
- Bioassay in one day chick I/M or I/P .
- Tissue culture on B or T lymphocytes .
- ECE 12-16 day >> dead hemorrhagic embryo .
 Detection : PCR and ELISA
Ab detection after 35 days .
Vaccines :
Depend only on cellular immunity .
Live attenuated vaccine only 3-4 w before laying for breeders only.
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‫‪82‬‬
virus age mortality Clinical signs PM Lab
curve
Deferential diagnosis of Diseases cause immune-suppression
IBHV 3-7 w MAX Mort 30% As CAV Pale comb and wattle . ECE :curling and
Peak in 3-4 d - liver : enlarged , pale hemorrhagic dwarfing.
from CS and IN inclusion bodies.
& stop 5 d – 3 w friable . serology
-Kidney : enlarged + hemorrhagic . -
bone marrow : watery and bale -
Atrophied bursa and thymus. -
hemorrhagic syndrome
IBDV 3-5 w Mort 1-70% sudden onset . Bursa : edematous>hemmo>atrophy Isolation : chicken
and hemorrhagic syndrome
peak 2-3 d from perfuse watery Nephrosis embryo bursal

CS diarrhea . Necrotic foci on spleen cells >plaque under
And stop after 9 picking of vent . Hemorrhagic syndrome agar
d Ag ( not Ab ) catch by
serology
CAV 2-4w Mortality 10-30% general + anemic Pale gelatinous bone marrow. Tissue culture on B or
2 peaks of comp, wattle , eye Atrophied thymus + ( transient T
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mortality at lids and legs + atrophied lymphocytes .
15 d 21 d petechiation and bursa ) ECE 16-120 day >>

Stop 3 w after CS ecchymosis Blue wing disease . dead
Hemorrhagic syndrome. hemorrhagic embryo
all Sudden death Sudden death – Hemorrhages PCR
HA >> HI ELISA ( Ab
and
vNDV
High mortality green diarrhea -Tips of provectriculus glands after 35 d )
rRT-PCR
100% –respiratory -Buttom shape Hemorrhages in
Peak in 3-4 d Of manifestation duodenum
CS Nervous -Cecal tonsils
manifestation -Rectum : zebra marking
Hemorrhages
Septicemi
HPAI all Sudden d High Sudden death – Hemorrhagic syndrome HA >> HI +
mortality green diarrhea – Respiratory and genital system rRT-PCR
100% respiratory inflammation
In 3-d days manifestation – Thymus,bursa atrophy
Cyanosis Septicemia
Nervous Hemorrhagic syndrome.
manifestation
Chapter 7 : Diseases causing

respiratory manifestation
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Avian pnoumovirus( APV )
= Turkey rhinotrachitis (TRT)
= swollen head syndrome(SHS)
Def : acute infection with paramyxovirus infect mainly Turkey and chicken , causing upper respiratory
manifestation with decrease in egg production .
Epidemiology :
Etiology :
Paramyxoviridae with no HAN ( non-heamagglutinating ) ( enveloped ) .
Classification :
Type A : UK isolates .
Type B : ( European isolates) . produce limited Ab against type A .
Spp. susceptible :
Only Turkey and chicken at any age but sever at youngs .
Need predisposing factor ( usually manegmental than infectious ) .
Transmission :
Direct and indirect airborne infection .
IP : 2-4 hours ( fastest virus ) .
CS ( respiratory complicating virus)

Young turkey ( poults). Laying Turkey .
Upper respiratory + frothy conjunctivitis. Less respiratory manifestation .
SHS Drop in egg quantity and quality up to 70% >>
Mortality : 4-90% acc 2ry infection . >> pneumonia and recover in 3 weeks.
torticollis .
Broiler chicken Layers and breeders
Upper respiratory + frothy conjunctivitis. As broilers + mortality 1-20% acc 2ry infection .
SHS and 2ry pneumonia and torticollis and cerebral Drop in egg quantity and quality.
disorientation
Mortality : 4-90%
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PM
Mucoid trachitis + SHS + panopthalmia + 2ry res bacteria CRD . Oophoritis
Pattern of CS :
 Predisposing to manegmental factor

 First week : APV CS only .
 Second week : APV + 2ry inf .
 Third week : 2ry inf only .
Diagnosis :
CH – CS – PM
Sampling : upper respiratory tract swaps or organs within first 2 weeks of infection .
Isolation : tracheal cell culture or QT-35 >> cell necrosis and syncytia .
Turkey embryo.>> death .
Identification : PCR – ELISA .
Vaccination :
1- Live attenuated : for TRT at day 1 , 7 , and 3-6 w .
2- Inactivated : after live attenuated .
- I/ M after last live attenuated 4-6 w .
- 4 weeks before laying .
- Used during laying .
TTT :
The relieve of the predisposing factor with antibiotic will solve the problem .
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Egg drop syndrome ( EDS ) :

Def : acute infection of laying chicken chch by mild respiratory signs followed by change in egg color,
quality and quantity with drop of egg production 10-20% .
Epidemiology :
Etiology :
 One serotype but 2 isolates >> EDS 76 ( in chicken ) – BC 14 ( buffy coat in fowls ).
Affected spp :
 Natural host : duck and geese

 Most affect broiler breeders and heavy breeds producing brown eggs.
Tropism : shell gland ( production of shell and pigments ) .
Transmission :
 Vertical .
 Horizontal : in chicken and water fowls.
CS :
 Respiratory manifestation .
 Chang egg color .
 Rough shell >> soft shell>> shell – less
 No change in hatchability and fertility .
 No mortality .
 Drop in egg production up to 50%
PM :
 Atrophied oviduct . normal ovary .
 Shell gland inflammation
 Enlarged mottled spleen .
 Ova in different size in abdomen .
Vaccination :
Only inactivated vaccine 4-6 w before laying .
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Infectious bronchitis (IB):

Infectious bronchitis (IB):
Def: acute highly contagious dis. Caused by coronavirus, affect mainly chicken chch by :
1- Upper respiratory manifestation.

2- Kidney affection in young.
3- Decrease quality and quantity of eggs.
Epidemiology:
Etiology
Coronaviridae virus ( SS RNA – round or pleomorphic – enveloped ).( no AG relationship ).
4 structural proteins :
1- : attachment and fusion of virus into the cell

Production of immune response .
Any change in it cause new variants ( responsible for mutation and identification ) .
2- Membrane glycoprotein ( N ).
3- Small membrane protein ( E) .
4- Internal nucleoprotein ( N) .
Classification :
1- Respiratory strain ( as H120) - nephrogenic ( variant ) strains as Gray and china QX

2- Classical and variant strains
Disinfection
As enveloped virus , any fat solvent will destroy it (AS chloroform and ether ) .
T-> 56 c for 15 min .
Natural hosts :
Only chicken , all ages are susceptible but adults resist:
nephrogenic strains – oviduct lesion – mortality due to infection .
baby chick more affected .
Transmission :
1- No vertical transmission , but the virus sheds on the egg shell in infected birds .
2- Horizontal :
- Airborne
- Feces as cecal tonsils carry infection 12-20 weeks .
- The recovered bird ( apparently healthy ) sheds the virus for 163 days - > carrier
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IP : 1-3 days
morbidity 100%
morbidity : - young less than 6 w : 30%
- mixed infection : increase severity , duration and mortality .
Clinical signs :
Broilers :
 Upper respiratory manifestation .

 Nephrogenic manifestation with or after the respiratory manifestation.
 Above 6 w ( and layers ) unnoticed respiratory manifestation , and no Nephrogenic
manifestation
Layers :
 Decrease egg quality ( egg deformities as small – pale – depigmented – rough – misshaped,
shell-less with inferior albumen quality and broken chalaza) and quantity ( 50% and usually
never regain the full production ) .
Day old chick (shell or airborne ) :
 Permanent damage to oviduct which cause ( at maturity ) normal ovulation with no catching of
the ova in infundibulum, so the hen take the motion of oviposition and fails to lay the egg which
call ( FALSE LAYING ) , the ovulated ova cause egg peritonitis .
PM :
In broilers :
- caseous plug at tracheal bifurcation .
- Serous , catarrhal or caseus exudate in respiratory tract .

- 2ry inf cause air-saccalitis and pneumonia .
- Nephritis with ureters distended with urates .
Layers :
- Egg peritonitis .
- Permanent change in oviduct specially mid-third .
- Pale pectoral Ms with gelatinous edema .
Cause of death :
asphyxia and dehydration in broilers – egg peritonitis in layers > both 2ry bacterial infection .
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Factors influencing disease :

1- Inc. stocking density.
2- Other respiratory dis .
3- Immune suppressive dis .
4- Increase protein level in ration . ( nephrogenic strain ) .
Diagnosis :
 Case history – Clinical signs – PM
 Sampling : cecal tonsils, kidney – oviduct ( make sterile suspension ) .
 Isolation :
1- In tracheal tissue culture .
2- 9-11 day old ECE >> serial blind passage : +ve if curling and dwarfing .
3- Intra-tracheal inoculation in baby chicks >> give CS after 1-3 days .
 Detection : ( to detect the serotype as it is useful in vaccination ) .
- VN- HI – immune florescence – immune peroxidase .
- Elisa for accurate detection of the serotypes .
DD:
diseases causes respiratory and nephrogenic manifestation in broilers .
Diseases causing decrease in egg quality and quantity .
Vaccine:
Maternal immunity doesn’t affect the vaccine
1- Live attenuated vaccine ( classical or classical and variant ) .

- Day 1 as spray
- Day 6-7 in drinking water or eye drops ( as hitchner IB )
- Before laying by 10-11 w
2- Inactivated virus :
- At day 11-12 with NDV or AI
- At 2-3 W before laying usually with NDV or ( IB+ IBDV + REO )
TTT: supportive TTT

1- Bronchodilator as mentophen.
2- Antibiotic ( not affect kidney ) as tylosine or Enrofloxacine .
3- Immune stimulant ( vit E sel ) .
4- Decrease protein in ration .
5- Increase T by 2 degree .
6- Electrolytes replacers . Renal wash .
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Infectious
Infectious laryngotrachitis(
laryngotrachitis( ILTILT
) )
Def: acute or subacute viral dis of chicken and fowls at older ages cause :
1- Mortality due to respiratory manifestation .
2- 2- dec. in egg production .
Epidemiology:
Etiology:
Herpes virus ( ds DNA – non enveloped ) ( antigenically homogenous = cross immunity )
Classification:
High virulent: high morbidity and mortality.
low virulent: low morbidity and mortality.
natural hosts:
adult chicken and fowls mainly ( all ages are susceptible )( upper respiratory tract only )
transmission:
only horizontal by:
- Airborne and fomites

- Latent Carriers : as recovered and vaccinated birds sheds the virus and latency occurred in
trigeminal ganglia in brain .
- Vectors: cats , rats , dogs and insects .
IP : 6-12 D .
C.S – morbidity and mortality . PM

form morb mort CS PM
Mild ( subacute ) 5% 1-2% Upper respiratory manifest. Upper respiratory inflammation .
Dec. egg quantity only .
Sever ( acute ) 100% 10- Upper respiratory manifest. Mucoid to hemorrhagic trachitis
20 % + hemorrhagic conjunctivitis. and laryngitis forming diphtheric
+ bloody cough . membranes .
Tracheal lumen filled with exudate
lead to suffocation .
Cause of death : suffocation or secondary bacterial inf.
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Diagnosis :
CS- CH –PM
Sampling : tracheal or conjunctival swaps or tissue .
Isolation : ON ECE : on CAM = pock lesion
Detection: 1- I/N inclusions >>>>> 2- serology ( Elisa ) >>> rapid : PCR , FAT , immune peroxidase .
Immunity and vaccination :

Depend on cellular immunity only >> live attenuated only .
Vaccinated birds shed the virus , so it is applied on endemic areas only .
Can be emergency vaccined .
At 7 and 15 w spray or eye drop or drinking water .
TTT: As IB but add vit K and emergency vaccination .
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‫‪100‬‬
‫‪chapter 8 : Rabbit diseases‬‬
‫‪101‬‬
Viral hemorrhagic disease(VHD)

Rabbit VHD (RVHD) viral hepatitis , hemorrhagic hepatitis, X disease
Def :acute, subacute or chronic viral disease of rabbit more than 6-8 w chch by nervous manifestation
, bloody nasal discharge and hemorrhages through the body organs (specially liver ) and mucous
membranes .
Epidemiology :
Cause :
Family caliciviridae , genus lagovirus (SS RNA – nonenveloped – resist freezing )
Classification :
- Classic RHDV : with 5 genotypes G1-G5

- Variant RHDV a/G6
- RHDV2
Transmission :
- Direct by : oral , nasal , conjunctival routs . ( infected animal or carcass or fomites as virus
excreta from all body secretions )
- Indirect :
 Vectors : wild animals ( by eating infected rabbit carcass ) and insect mechanically. Specially
during viremia .
 Frozen meet can transmit it to new areas.
IP : 1-5 d morbidity : 100% mortality : 70-90% starts after 12-36h after fever >40 C .
Pathogenesis and age susceptibility:

After transmission , the virus replicate in reticulo-endothelial system , followed by infecting all the body
cells specially hepatocytes as it contain transaminase enzyme to replicate , however this enzyme
present in very low amount in youngs less than 4-6 weeks at which the age resistance occur .
After liver infection , the virus undergoes viremia and intravascular coagulation in all the body occur ,
lead to rupture of the blood vessels , including brain BVs , which appear as multiple hemorrhages in the
body and nervous signs, death occur due to coagulopathy .
102
Clinical CS PM
form
Per-acute Sudden death with no CS or CHCH PM but pyrexia (41-42 ) may occur and stomach is full
with food and rectum full with hard fecal matter .
Acute Anorexia , apathy , dullness , prostration Liver necrosis ( yellowish brown , degenerated )
, nervous signs , pyrexia , respiratory Splenomegaly .
disturbance and bloody nasal discharge . Trachea contain frothy bloody discharge .
Cyanosis of MM . Clotted blood in BVs and multiple hemorrhages.
Sub-acute As acute but milder + agonal vocalization Ichtrus in ears and conjunctiva is prominent
+ obvious opisthotonos . As acute but milder
Chronic Jaundice and weight loss Ichtrus in ears and conjunctiva is prominent
Die within 1-3 w from liver dysfunction
DD : septicemic pasteurellosis , poisoning and heat stasis .
Diagnosis : CS , PM
Sampling : liver , spleen , then all secretions and excretions .
Identification :
1- HA : performed by 10% liver or spleen homogenate + human type O RBCs

2- Elisa
3- EM
4- RT-PCR
5- Serology . ( Ab detection 7 days after infection )
6- Histopathology .
No TTT
Prevention :
1- Hygienic measures .
2- Not import from endemic areas .
3- Use specific disinfectants ( phenol and soda ) + arthropod control.
4- Vaccination .
Vaccination :
In Egypt :
 Inactivated formalizes ( or b-bromolactone ) vaccine :

For breeders at 4w and before breeding 4-6 w .
 Recumbent vaccine with myxomavirus inj .
 MDA = 4-8 w .
Only in UK : live attenuated vaccine , why not used ??
1- Hard to grow in tissue culture .

2- Pathogenicity at aged animals .
103
Myxomatosis
Mosquito disease – big head disease
Def : acute fetal viral disease of young rabbits mainly , chch by S/C edema specially on head .
Epidemiology :
Myxomavirus ( DS DNA – enveloped ) .
Transmission :
Direct – indirect by mosquito vectors .
IP : 1-3 W
Early stage In survivors
CS edema in eye , lips nose , ear till it become heavy and S/C gelatinous tumors all over the
pendulous ( big head disease ) body .
edema in genital region >> infertility for 1 year .
Pyrexia.
Mucopurulent discharge from eye and nostrils.
Occasionally . in acute cases , sudden death with slight
conjunctival inflammation and pyrexia (42.5)
PM Consolidation and congestion of lung.
Enlarged dark red spleen .
S/C edema is clear and gelatinous ( fibrinous in pastuerella )
Microscopic : large eosinophilic cytoplasmic IB in conjunctival membranes .
Diagnosis :
CS , PM , I/C IB are evidence .
Serology : can detect Ab 7-28 days post infection .
Prevention and control:

1- Antibiotic + fluid therapy + NSAIDs
2- Arthropods control
3- Hygienic disposal of dead animals .
4- Vaccination : live attenuated or recombinant vaccines with RHDV .
MDA : 5 w .
Parental resistance : recovered male give resistance to offspring for 4-5 w . ‫نظريه مش مؤكده‬
104
Rabbit pox
 Rare disease can occur without CS .
 If CS occur it will be : lymphadenitis , popular nodules on mucous membranes , and orchitis
 Mortality 75% in unweaned rabbits
 Vaccine with vaccinia virus .
Coccdiosis :
Cause Eimeria spp
Life cycle Sporulated Oocyct >> ingestion >> sporozoit >> merozoit >> gametes >> zygote >
unsporulated oocyct >> in worm+ humidity + oxygen >> sporulated Oocyst
Age Most suciptable in 1-3 w
Form Hepatic coccidiosis Intestinal coccidiosis
Cause E. stiedae E. magna , Eirresidua are most dangerous.
Then E. intestinalis, media …etc .
CS - Jaundice - Diarrhea (bloody )
- Anorexia - Anorexia
- Rough coat - Weight loss
- Weight loss - Dehydration
- May be with diarrhea (not common )
- Usually sub-clinical
pm Yellow white nodules in liver Small whitish spots on intestines develop
Enlarged liver to thick intestinal wall > grayish white
streaks.
Diagnosis PM -Liver impression smears on L/M .
Fecal floatation or gall bladder L/M all for demonstration of Oocytes
Prevention Clean food and water
Dry hatches
Remove feces
Disinfection by Amm, solution or NaOH 10%
Rearing on cages
TTT Sulphaquenoxaline or toultrazoril in drinking water (30 d course ) or feed ( 20 day course ) 2
days every 8 days or 5 days every 10 days in heavy infection ,
Arthropodes :
1) Rabbit flea :
 Spilopsyllus cuniculi
 Cause irritation and alopecia in ear
 Transmit myxomatosis
105
2) Arachnids :
A) Body mange :
 Sarcoptes scabei or notoedres cati
 Fetal disease , barrow in skin and lay eggs >> puritis
 Zoonotic
 CS and PM : alopecia , puritis on face near lips >> if fall to all the body >> no TTT
 Diagnosis : skin scraping and CS and PM .
 TTT : must be early
- Clipping of fur
- Mild antiseptic solution to remove scapes .
- Apply sulpher ointement .
- Ivermectine 0.4 mg / Kg 3 times 14 days interval . ( not in pregnant ).
B)Ear mange or ear canker

 Psorobtes , non borrowing , inside ear pinna .
 Cause irritation to make rabbit scrape it self > injury > blood ( nutrients ) material.
 PM : Brown crusts inside ears . Otitis externa
Secondary infection to middle ear and brain >> nervous manifestation .
 Diagnosis : CS , PM , LM
 TTT :
- Removal of crust with disinfectant .
- H2O2
- Liquid paraffin + phenol 1%
- Ivermectine
- Antibiotics
Pin worm
No CS – TTT by peprazine 0.5 mg/kg or ivermectine .
Cestodes :
Intermediate host of tenia serialis and pisiforms .
Migrate to liver and under skin and leave white tortuous subscapular tracts
No CS except under weight
Lesions : cesticercus attached to mesentery
TTT mebendazole 50 mg/Kg for 14 w .
106
Microsporidium
Encephalitozoon cuniculi
MOT : spores in urine + experimentally aerosols .
Zoonotic for immune suppressed human.
Life cycle > spores in urine > inter the body > sporoblasm > sporoblast > spors in urine .
Cs: subclinical or chronic in nature
Nephropathy : swollen kidney + subcortical depression.
Diagnosis :
 histopathology of brain and kidney 9 focal granulomatous lesion or spores inside glia cells.
 Granulomatous interstitial lesion in kidney .
 Cyst in kidney and brain
 Serology as Ab production starts 1 month before shrdding .
TTT : No TTT or vaccine only supportive TTT by folic acid , pyrimethamins and sulphadiazine .
107
‫‪Chapter 9 : water fowls‬‬

‫‪viral diseases‬‬
‫‪108‬‬
Viral Infections of Waterfowl

Interests in viral infections of waterfowl are more diverse than for poultry and focus on 3
different issues:
(1) problems associated with raising birds commercially,
(2) problems associated with wild waterfowl, and
(3) problems created by migratory waterfowl in the transmission of infectious disease to
commercially reared waterfowl and poultry.
 RNA viruses associated with waterfowl include Picornaviridae (DHA, duck picornavirus
[DPV]), Astroviridae (DHV II and III), Paramyxoviridae (avian metapneumovirus, avian
paramyxoviruses (1, 4, 6, 8, and 9), Orthomyxoviridae (avian influenza), Flaviviridae (West Nile
virus), and Reoviridae (Duck reovirus, Muscovy duck reovirus and goose reovirus).
 DNA viruses include Herpesviridae (DVE, goose herpes virus), Adenoviridae (duck
adenovirus), Circoviridae (circovirus-like infection of ducks and geese), Hepadnaviridae (duck
hepatitis B virus), Parvoviridae (MDPV and GPV), and Polyomaviridae (GHPV).
Duck Hepatitis (DH)

Def : is a highly fatal, rapidly spreading viral infection of young ducklings characterized primarily by
hepatitis.
Epidemiology :
Cause :
Picornavirus genus (Avihepatovirus)
Classification :
 duck hepatitis A virus 1 (DHAV-1) +A variant strain named DHAV-1a

 DHAV-2 ( Duck Astrovirus types 1)
 DHAV-3 ( Duck Astrovirus type 2)
109
Duck Hepatitis Type 1

Chemical and physical susceptibility :
 inactivated at 56°C after 30 minutes, and survive for longer period in cooler T .( heat stable)
 resist disinfectants .
Transmission :
Direct and indirect contact by aerosol and orofecal routs .
IP : 1-2 d
Morbidity is 100%
Mortality : according age : if < 1 w = 95% if 1-3 w = 50% if 4-5 w = low .
CS PM
-Very rapid onset as all mortality occurring within 3–4 -Liver enlarged contains punctate or ecchymotic
days. Death occurs within an hour of CS onset . hemorrhages + reddish discoloration or mottling of
-stop moving and squat down with eyes partially the liver surface.
closed -Spleen enlarged and mottled.
-fall on their sides, kick spasmodically with both legs , -Kidneys : swollen and renal blood vessels congested.
then die .
Immunity :
 recovery results in solid immunity and VN antibodies in the serum .
 Active immunity can be induced in adult ducks by injection of certain strains of virus.
Some strains require repeated injections to obtain high levels of antibody .
 Passive immunity : in yolk or by injection serum of recovered ducks .
Diagnosis :
1- Inoculation
 SC or IM of the isolate into 7-day-old DHAV susceptible ducklings >> 24h CS + PM then continue
 serial dilutions of the liver homogenate into the allantoic sacs of embryonating duck eggs (aged
10–14days) from a DHAV-free flock >> die within 24–72 h or
chicken egg (8–10 d) die within 5-8 d ,, lesions include :
- allantoic fluid is opalescent or a pale greenish-yellow.
- include stunting and subcutaneous hemorrhages over the whole body, with ascites .
- liver swollen, red, and yellowish in color,and show necrotic foci.
 duck embryo liver cells or DEK >> CPE which cell rounding and necrosis, or plaques with a
maintenance medium containing 1% agarose . followed by FAT .
2- RT-PCR and Multiplex PCR ( detection and differentiation of DHAV types)
3- Serology : not useful in diagnosis but used identification, titration of serologic response to
vaccinations .
110
Differential Diagnosis : ‫مهم‬
 The sudden onset, rapid spread, and acute course of the disease are characteristic in this age
For DVH , but diffecult to DD DHAV 1 from the other DHAV 3 and 2.
 acute mortality in ducklings include salmonellosis and aflatoxicosis , The latter disease may
cause ataxia, convulsions, and opisthotonos , but does not cause the same characteristic liver
hemorrhages. None of the other common lethal diseases of ducks occur in this young age group.
Prevention & Control :
1- Management Procedures : strict isolation, particularly during the first 4–5 weeks of age.
2- Breeder vaccination .
Vaccination :
1- Live attenuated vaccines : by chicken embryo-passaged DHAV-1.
 In breeders : inoculate 0.5 mL undiluted egg-propagated virus intramuscularly 2–4 weeks before
collecting hatching eggs but repeated injections necessary to obtain sufficient antibody levels to
protect hatched ducklings ( two doses 6 week apart ) .
 Ducklings : by foot web-stab , IM , orally, eye-drop route ( even in one day old ) and aerosol .
2- inactivated vaccines :
 three doses of inactivated oil-emulsion vaccine .
 live DHAV-1 vaccine at 2–3 days of age, followed by inactivated vaccine at 22 weeks, produced
significantly higher VN antibody.
Treatment:
Injection of 0.5 hyperimmune serum to each duck .
injection of yolk from eggs produced by hyperimmune breeder ducks.
111
Duck Hepatitis Type 2 Duck Hepatitis Type 3

etiology Duck Astrovirus types 1 Duck Astrovirus types 2
Spp affected Only ducks (wild birds vectors )
transmission oral, cloacal, and subcutaneous routes
IP 1–4 days
Mortality 10% and 25% in 3- to 6-week-old mortality rarely exceeded 30%
50% in 6- to 14-day-old birds.
CS polydypsia with loose droppings, As DHAV-1
excessive urate excretion, and sometimes
convulsions and acute opisthotonos.
ucks usually die in good condition 1–2
hours after the appearance of CS
PM pale pink with multiple, small punctate As DHAV-1
hemorrhages.
spleen is invariably enlarged and
“sago-like” in appearance due to
scattered pale foci.
Kidney swollen and congested.
Occasionally, small hemorrhages are seen
in the intestinal wall and on the heart fat.
diagnosis EM examination of liver homogenates tentative identification can be by inoculation
Isolation : very hard on ECE and EDE intra of liver suspension onto the CAM of 10-day-old
alantoic after repeated passage > embryonating duck eggs if embryo
mortality up to 20% may occur within 2–4 lesions and mortality patterns as adults .
days PI EM or PCR
No isolation on tissue culture
TTT convalescent serum obtained from DHV Convalescent sera obtained from DHV type 3-
type 2-infected ducks infected ducks
112
Duck Virus Enteritis (Duck Plague)

Def : acute, contagious herpesvirus infection of ducks, geese, and swans, characterized by vascular
damage, tissue hemorrhages, digestive mucosal eruptions, lesions of lymphoid organs, and
degenerative changes in parenchymatous organs.
Epidemiology :
Herpesvirus ( DS DNA non enveloped ) .
Afeect macrophages and epithelial cells of GIT , as well as liver , spleen , thymus and bursa .
Spp affected : ducks, geese, and swans( High incidence of DVE was noted in spring)
Transmission:
Direct and indirect orofecal specially in water
Blood sucking arthropods .
IP : 3–7 days, death follow CS after 1-5 days .
Mortality : 5%–100% ( Adult breeder ducks tend to experience higher mortality than young ducks.)
In domestic breeder ducks Young ducklings

CS sudden, high, persistent flock mortality . 2–7 weeks
Mature ducks die in good flesh (males ) dehydration, loss of weight,
marked drop in egg production. blue beaks,
Photophobia conjunctivitis, lacrimation, nasal exudate,
Ataxia , soiled vents,and watery diarrhea. and often a blood-stained vent.
unable to stand; show tremors of head,
neck, and body.
PM *disseminated intravascular GIT : sloughing
coagulopathy and necrotic degenerative of the entire mucosa forming thick
changes in mucosa and submucosa of yellow-white membrane
GIT, in lymphoid and parenchymatous Meckel’s diverticulum maybe
organs Hemorrhagic.
*hemorrhages on myocardium , serous In ceca, rectum and vent : macules are
membranes epicardium giving observed , densely packed > red > plaque-
paintbrush” appearance + endocardial like elevations become green and form a
mural and valvular hemorrhages. continuous scale-like band.
*Petichiation on the internal organs & SI . Late stages of infection are characterized by
* deformed, discolored ovarian dark bronze or bile-stained livers or pale
Follicles. copper color with hemorrhages firstly , then
* The esophageal-proventricular without hemorrhagesthen white foci are
sphincter appears as a hemorrhagic ring. Atrophied thymus bursa and spleen .
cavity. Lumina of intestines and gizzard
are often filled with blood.
*Diphthreic membranes ( yellow to green
)In GIT .
Atrophied thymus bursa and spleen .
113
Diagnosis :
Sampling : liver, spleen, bursa, kidneys, peripheral blood lymphocytes (PBL), and cloacal swabs.
Isolation : EDE or ECE >> on cam >> pock lesion + other DVE signs .
Muscovy duck emryo fibrobasts + serology .
Identification :
Latex agglutination test, Elisa PCR , FAT , VN with index 1.75 or more ‫احفظها لو جت اختياري مثالااا‬
An immunochromatographic strip :
use as a field test for monitoring flock immunity post vaccination and detection of expo-sure to DEV
in unvaccinated flocks. This test is easy to perform, rapid (15 minutes), specific, and with equal
sensitivity as the antibody ELISA.
Vaccination :
A live attenuated chicken embryo-adapted DEV strain, (avirulent).( prevent infection and used in
emergency vaccination by interferons production )
A live attenuated naturally apathogenic and immunogenic strain of DVE.( preventive only ) .
Inactivated vaccine also present , but live attenuated is much protective than it
114
Hemorrhagic Nephritis Enteritis of Geese (Goose polyomavirosis.)

Cause :
Polyomaviridae family and Polyomavirus genus (DS DNA non enveloped ) .
resistant to all of heat, freezing-thawing cycles and lipid solvents.
Incubation Period mostly age dependent:
1 d > death within 6-80days
3w > IP 15 d
More than 4 w > non clinical infection
goslings from 4–10 weeks of age is affected ( have CS ) .
transmission : orofecal .
morbidity : 10%–80
CS :
signs develop rapidly only a few hours before death
Nervous signs, such as opistothonos,
Chronic evolution of the disease leads to urate deposits on viscera and in joints, resulting in lameness
with limited mortality .
Lesions: edema in S/C , gelatinous ascites , nephritis , hemorrhagic enteritis , visceral gout , articular
gout .
Diagnosis :
Isolation could be based on either kidney cell culture or goose embryo inoculation.
PCR : designed on VP1 gene is efficient and reliable.
subclincally infected carriers : carriers, PCR assays can be advantageously performed on blood samples
or spleen or cloacal swabs.
ELISA has been developed using viral antigens or recombinant VP1.
Serology appears of limited value
Differential Diagnosis : goose parvovirus infections .
Vaccination:
1- autogenous inactivated, and alumin-adjuaned for breeders and gooslings .

2- subunite vaccine with VP1 on E.coli .
115
Goose Parvovirus Infections (Derzsy’s disease, goose influenza)

Def :acute, subacute or chronic highly contagious fatal disease affecting young geese and Muscovy
ducks.
Cause : Parvoviridae ( SS DNA non enveloped )

Classification : goose parvovirus (GPV) both in goslings and ducklings, and duck parvovirus (MDPV)
only in Muscovy ducks. The age of infection from 1 – 4 weeks , above 5 w are negligible.
Mortality : acute form of the disease can result in 100% mortality in gosling less than 10 days of
age.
Infection in the hatcheries or at less than 1 week of age can result in 100% mortality .
over 4 weeks of age rarely show clinical signs .
Transmission :
vertical and horizontal by orofecal and latent birds .
Incubation Period : first w > 3-5 days ….. 2nd and 3rd week >> 5-10 d and increase in males .
Clinical Signs :
In the acute form : general signes then die within a few days. nasal and ocular discharge, conjunctivitis,
profuse white diarrhea, and loss of natal down. Some of these birds have mucosal necrosis and a
fibrinous pseudomembrane covering the tongue and oral cavity.
In birds that survive the acute phase and in those that develop a more prolonged form :
reduced feed intake, profound growth retardation, and loss of feathers on the back and neck.
Ascetis, causing the goslings to stand in a ‘penguin-like posture’.
In Muscovy ducks :
ducks, locomotors problems including weak-ness, lateral recumbence, and inability to walk
growth retardation, short beak , and the shortening of the leg bones, with a low morbidity.
Gross Lesions
In acute cases : hepatomegaly with fibrinous periheptitis . , pale myocardium, and dilatation of the
Heart. + ascites
In the acute enteric form of the disease : severe necrotic enteritis with diphtheritic lesion in the small
intestine , Diphtheritic and ulcerative lesions in the mouth and pharynx.
116
In a more prolonged clinical course : the birds lose their feathers, especially on the back, neck, and wing,
and have markedly reduced body weight.
In Muscovy ducks: pale thigh and heart muscles, increased pericardial fluid, serofibrinous perihepatitis,
and ascites.
Diagnosis :
Isolation and Identification of the Causative Agent :
embryonated goose or Muscovy duck 10- to 15-day-old inoculated via the allantoic cavity mortality
occurs 5–10 days post inoculation with liver lesions and hemorrhages on the skin.
tissue cultures prepared from duck or goose : produces a well defined cytopathic effect 3–5 days PI .
Direct Detection of Viral Antigen :
IFAT , immunoperoxidase , Flow cytometry assay to detect virus-infected cells in the spleen.
Electron Microscopy .
Molecular Identification : PCR, RT- PCR
Differentiation of GPV and DPV can be done by restriction fragment length polymorphism (RFLP) or
nucleic acid sequencing.
Nucleotide sequence analysis of capsid protein genes of GPV allows the differentiation of vaccine and
wild strains
thermal amplification based method has been developed for simple, rapid
detection of waterfowl parvoviruses, but this method cannot differentiate strains.
Serology : ELISA
Vaccination:
MDA : 2-4 w
hyperimmune or convalescence serum injected subcutaneously in day old goslings.
Live vaccines containing attenuated goose parvovirus : interfere with MDA .
Inactivated vaccines containing the whole parvovirus antigens, either in the monovalent (GPV) or
bivalent (GPV and MDPV) forms,
Vaccination at 1–2 weeks .
117

Final Poultry Disease Coulored Demo

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‫ حقوق البيع ترجع للكاتب‬...

‫نسخه عرض غير مخصصه للبيع‬

Poultry and rabbit diseases

Dr/Muhammed Abd-Alfattah Muhammed

Table of the contents

Chapter 8 : Rabbit viral and parasitic disease

Virus is a small infectious agent that replicates only inside

- Enveloped viruses in poultry includes : AI , NDV , APV and IBV .

In each virus there are main points will be:

e- chemical and physical resistance :

- enveloped viruses can destroyed by environmental conditions as sun light or humidity

 Venereal : from male to female then offspring : CAV .

3- incubation period : time elapsed from infection till clinical signs .

4-Morbidity : % infected birds in the flock .

5-Mortality : % dead bird in the flock .

6- Clinical signs : includes :

7- PM : vary according virus .

9-Vaccination and immunity :

 Live vaccine : used to produce cellular immunity .

10-Prevention : biosecurity , good management , vaccination .

11-Control : isolation and culling , : biosecurity , good management ,emergency vaccination.

Avian immunology and vaccination concepts

•The immune system characterized by:

1- Discriminates self from non-self

Cells of the immune system :

phagocytic phamily lymphoid family

Tissues of immune system :

2- payer patches in duodenum .

5-Others ( GALT , SALT , MALT , BALT ) .

Organs of immune system :

1- Bursa of Fabricous : produce the steam cells + B-lymphocytes .

secondary lymphoid organs

Important in eye drop vaccination .

non spacific spacific

Non- specific immunity(innate immunity ) :

The role of the non- specific immunity in the production

1) T-cell identify the 2) secrete the lysis 3) the infected cell

 Clinical disease and mortality (AI, ND, IB,IBD).

vaccination of a bird is done in 3 stages :

 As AI , NDV and IB . ( MDA protection is only 5-7 days ) .

A number of factors should be considered in determining the best age to vaccinate:

 the initial quantity of MDA .

2- early active protective immunity :

3-late active protective immunity :

 Naturally weak as lentogenic strain of ND.

2- inactivated vaccines with oil emulsion or Al OH adjuvant:

 Doesn’t interfere with the virus MDA to be vaccinated .

 Not usually available .

Methods of vaccine application :

 Fowl pox vaccines or cholera..

 Conditions of emergency vaccines :

 Storage (vaccine delivery)

Factors related to the bird :

 Age (time of vacc.)

Vaccination schedule in broiler flock in general :

Other strategies according each virus in the viruses chapters .

chapter 2 : Avian parasitic disease

External parasites of poultry :

Disease causing nervous manifestation

 Piprazine compounds: affect adult so repeated every 2 weeks .

 Phenothiazine : alone or with piprazine 4:1 .

 Tincture iodine 1: 9 in water