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Dr Fares El-khayat  -Infectious bursal disease Slide 1 Dr Fares El-khayat  -Infectious bursal disease Slide 2 Dr Fares El-khayat  -Infectious bursal disease Slide 3 Dr Fares El-khayat  -Infectious bursal disease Slide 4 Dr Fares El-khayat  -Infectious bursal disease Slide 5 Dr Fares El-khayat  -Infectious bursal disease Slide 6 Dr Fares El-khayat  -Infectious bursal disease Slide 7 Dr Fares El-khayat  -Infectious bursal disease Slide 8 Dr Fares El-khayat  -Infectious bursal disease Slide 9 Dr Fares El-khayat  -Infectious bursal disease Slide 10 Dr Fares El-khayat  -Infectious bursal disease Slide 11 Dr Fares El-khayat  -Infectious bursal disease Slide 12 Dr Fares El-khayat  -Infectious bursal disease Slide 13 Dr Fares El-khayat  -Infectious bursal disease Slide 14 Dr Fares El-khayat  -Infectious bursal disease Slide 15 Dr Fares El-khayat  -Infectious bursal disease Slide 16 Dr Fares El-khayat  -Infectious bursal disease Slide 17 Dr Fares El-khayat  -Infectious bursal disease Slide 18 Dr Fares El-khayat  -Infectious bursal disease Slide 19 Dr Fares El-khayat  -Infectious bursal disease Slide 20 Dr Fares El-khayat  -Infectious bursal disease Slide 21 Dr Fares El-khayat  -Infectious bursal disease Slide 22 Dr Fares El-khayat  -Infectious bursal disease Slide 23 Dr Fares El-khayat  -Infectious bursal disease Slide 24 Dr Fares El-khayat  -Infectious bursal disease Slide 25 Dr Fares El-khayat  -Infectious bursal disease Slide 26 Dr Fares El-khayat  -Infectious bursal disease Slide 27 Dr Fares El-khayat  -Infectious bursal disease Slide 28 Dr Fares El-khayat  -Infectious bursal disease Slide 29 Dr Fares El-khayat  -Infectious bursal disease Slide 30 Dr Fares El-khayat  -Infectious bursal disease Slide 31 Dr Fares El-khayat  -Infectious bursal disease Slide 32 Dr Fares El-khayat  -Infectious bursal disease Slide 33 Dr Fares El-khayat  -Infectious bursal disease Slide 34 Dr Fares El-khayat  -Infectious bursal disease Slide 35 Dr Fares El-khayat  -Infectious bursal disease Slide 36 Dr Fares El-khayat  -Infectious bursal disease Slide 37 Dr Fares El-khayat  -Infectious bursal disease Slide 38 Dr Fares El-khayat  -Infectious bursal disease Slide 39 Dr Fares El-khayat  -Infectious bursal disease Slide 40 Dr Fares El-khayat  -Infectious bursal disease Slide 41 Dr Fares El-khayat  -Infectious bursal disease Slide 42 Dr Fares El-khayat  -Infectious bursal disease Slide 43 Dr Fares El-khayat  -Infectious bursal disease Slide 44 Dr Fares El-khayat  -Infectious bursal disease Slide 45 Dr Fares El-khayat  -Infectious bursal disease Slide 46 Dr Fares El-khayat  -Infectious bursal disease Slide 47 Dr Fares El-khayat  -Infectious bursal disease Slide 48 Dr Fares El-khayat  -Infectious bursal disease Slide 49 Dr Fares El-khayat  -Infectious bursal disease Slide 50 Dr Fares El-khayat  -Infectious bursal disease Slide 51 Dr Fares El-khayat  -Infectious bursal disease Slide 52 Dr Fares El-khayat  -Infectious bursal disease Slide 53 Dr Fares El-khayat  -Infectious bursal disease Slide 54 Dr Fares El-khayat  -Infectious bursal disease Slide 55 Dr Fares El-khayat  -Infectious bursal disease Slide 56 Dr Fares El-khayat  -Infectious bursal disease Slide 57 Dr Fares El-khayat  -Infectious bursal disease Slide 58 Dr Fares El-khayat  -Infectious bursal disease Slide 59 Dr Fares El-khayat  -Infectious bursal disease Slide 60 Dr Fares El-khayat  -Infectious bursal disease Slide 61 Dr Fares El-khayat  -Infectious bursal disease Slide 62 Dr Fares El-khayat  -Infectious bursal disease Slide 63 Dr Fares El-khayat  -Infectious bursal disease Slide 64 Dr Fares El-khayat  -Infectious bursal disease Slide 65 Dr Fares El-khayat  -Infectious bursal disease Slide 66 Dr Fares El-khayat  -Infectious bursal disease Slide 67 Dr Fares El-khayat  -Infectious bursal disease Slide 68 Dr Fares El-khayat  -Infectious bursal disease Slide 69 Dr Fares El-khayat  -Infectious bursal disease Slide 70 Dr Fares El-khayat  -Infectious bursal disease Slide 71 Dr Fares El-khayat  -Infectious bursal disease Slide 72 Dr Fares El-khayat  -Infectious bursal disease Slide 73 Dr Fares El-khayat  -Infectious bursal disease Slide 74 Dr Fares El-khayat  -Infectious bursal disease Slide 75 Dr Fares El-khayat  -Infectious bursal disease Slide 76 Dr Fares El-khayat  -Infectious bursal disease Slide 77 Dr Fares El-khayat  -Infectious bursal disease Slide 78 Dr Fares El-khayat  -Infectious bursal disease Slide 79 Dr Fares El-khayat  -Infectious bursal disease Slide 80 Dr Fares El-khayat  -Infectious bursal disease Slide 81 Dr Fares El-khayat  -Infectious bursal disease Slide 82 Dr Fares El-khayat  -Infectious bursal disease Slide 83 Dr Fares El-khayat  -Infectious bursal disease Slide 84 Dr Fares El-khayat  -Infectious bursal disease Slide 85 Dr Fares El-khayat  -Infectious bursal disease Slide 86 Dr Fares El-khayat  -Infectious bursal disease Slide 87 Dr Fares El-khayat  -Infectious bursal disease Slide 88 Dr Fares El-khayat  -Infectious bursal disease Slide 89 Dr Fares El-khayat  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Dr Fares El-khayat -Infectious bursal disease

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Dr Fares El-khayat -Infectious bursal disease

  1. 1. Infectious Bursal Disease Infectious Bursitis ‫المعدي‬ ‫البورصة‬ ‫التهاب‬ ‫المعدي‬ ‫فابريسي‬ ‫كيس‬ ‫التهاب‬ ‫الجمبورو‬ ‫مرض‬ ‫الدجاج‬ ‫ايدز‬
  2. 2. Historical informations: 1-First recorded as a specific disease in 1962 by Albert Cosgrove in the town of Gumboro, Delaware-USA and so known as Gumboro disease. 2-IBD was recorded for the first time in Egypt in 1974 by El-sergany et al. depending on the clinical and pathological investigation of the disease. 3-The very virulent strains of IBDV were first recorded in Egypt in 1989 by Khafagy et al. depending on the isolation and identification of the isolated strains. 4-The variant strains of IBDV are first recorded in Egypt in 2003 by El.Khayat depending on the direct isolation, serological identification and the application of Antigen-Capture ELISA “Monoclonal antibody” technique.
  3. 3. Definition: IBD is an acute, highly infectious and contagious disease of only young chickens (mostly 3-6 wk in age) and is characterized: Clinically by -Self-vent picking. -Profuse watery yellowish white diarrhea. -Tremor of the whole body. -Characteristic spiking curve of mortalities. Pathologically by -inflammatory enlargement of BF followed by atrophy. -edematous to hemorrhagic BF. -Ecchymotic hemorrhage on the lateral aspect of the thigh. -Peripheral yellow infarction. It is economically important to the poultry industry worldwide due to increased susceptibility to other diseases and negative interference with effective vaccination.
  4. 4. The economic importance of the disease is manifested in two ways: 1-The mortality, up to 20%, in chickens in the age of three weeks and older. 2-the severe, prolonged immunosupression of chickens infected at an early age. 3-the financial losses due to reduced production parameters as a result of sub-clinical infections.
  5. 5. Cause: Birnavirus → belonging to Birnaviridae -55-60 nm in diameter. -The genome is “bisegmented dsRNA genome”. IBDV has 2 segments of RNA “segment A and B”. -Birnaviruses have 4 structural proteins. VP1 (90,000), VP2 (41,000), VP3 (35,000) and VP4 (28,000). All of these viral proteins are immunogenic but VP2 is the only protectogenic one. -Has a predilection for lymphoid tissue, esp. Bursa of Fabricius “BF” and replicates in the immature bursal-derived lymphocytes (B- lymphocytes) causing immunosuppression that may be “either severe, prolonged if the chicks are infected earlier than 3 wks of age or moderate and transient if the chicks are infected post three wks of age. -Non-enveloped = naked → “highly resistant” to the physical & chemical disinfectants. IBDV is only sensitive to iodine, formalin and nascent oxygen compounds.
  6. 6. -It persists for a long period "more than 4 months” in poultry house and the surrounding environment. -Has two serotypes (Pathogenic serotype-1 & Non-pathogenic serotype-2). -Serotype-1 has 3 different subtypes or pathotypes of variable pathogenicity and global distribution: -Classic or virulent strains (e.g. strain 52/70) cause up to 50% mortality in SPF birds but only 1-2% in conventional commercial broiler chicks. -Very virulent strains, cause up to 100% mortality in SPF birds, 20-25% in commercial broiler chicks and 50-60% in commercial layers. They do not grow in cell culture unless propagated in cells such as chicken embryo fibroblasts for a number of passages to allow adaptation. -Variant strains causing less than 5% mortality without bursal lesions. Sometimes, a pathotype of viruses is identified with antigenic relation to both classic and variant viruses. Virulent serotype 1 strains induce both mortality & bursal lesions but their vaccines cause no mortality but possess residual pathogenicity with bursal lesions varying from mild to moderate or even severe. Serotype 2 strains cause neither mortality nor bursal lesions in SPF birds.
  7. 7. Susceptibility: Chicken are the only susceptible host for IBD . The main age of susceptibility is 3-6 wks of age with extremely rare clinical cases of IBD are recorded in an older ages. Baby chicks' future-layers are more susceptible than the commercial broiler chicks and the baby chicks' future-breeders. White baby chicks' future-layers are more susceptible than brown baby chicks' future-layers.
  8. 8. Source of Infection: -Infected birds… excrete the virus up to 2-3 wks. -The darkling beetles or "Lesser meal worm” = Alphatobious diapernus → → carry IBDV up to 8 wks. -Litter mites → → carry IBDV up to 8 wks. -Dogs…if eat infected birds. Mode of Infection: oral via ingestion of contaminated materials. Infection can take place via the respiration tract, and the eyes and by experiment via infection in the blood and via the cloaca. Mode of Transmission: -Direct contact between healthy and infected birds. -Indirect contact between healthy susceptible birds & the fomites of the infected birds. -Mechanical transmission via the contaminated feed, water and contact persons. -Mosquitoes are possible mode of transmission. -There is neither carrier state nor egg-transmission in IBD. -No air borne infections. Incubation period: Short I.P “2-3 day”.
  9. 9. Pathogenesis -After oral infection of the intestinal lymphoid tissues, virus reach the liver in 8-12 hrs post-infection. -From the liver, IBDV enters the blood stream and then infects the cloacal bursa (initial low-level viremia). -IBDV multiplies in the bursal and splenic macrophages after 24 hrs. It does not replicates in the peripheral lymphocytes. -It reaches the highest concentration in 4-5 days. -As the BF undergoes infection, the second, massive viremia occurs. -Antibodies against IBDV are detected as early as 3 days post- infection.
  10. 10. Forms of IBD There are 2 forms of IBD: Sub-clinical IBD: It occurs either due to infection of young birds with a variant IBDV strain at any time of age or infection of young birds with a classic strain of IBDV in age less than 3 wks. This occurs due to IBDV breaks through MDA. The degree of immunosuppression varies depending on the virulence of the virus strain and age of infection. It is greater the closer the infection occurs to hatch and because the birds are a young age, it is permanent hence; infected chickens with IBDV at 1-day old are completely devoid of IgG and produce only monomeric IgM. It has no clinical signs, no inflammatory bursal lesions although a rapid silent strong persistent immunosuppression occurs. Clinical IBD: here, infection of young birds with a classic strain of IBDV in age from 3-6 wks. It has obvious clinical signs and the morbidity may reach 100% of the flock and mortality can range from 0% to over 50% with very virulent IBDV (vvIBDV) strains. Immunosuppression is transient in the clinical form.
  11. 11. 0 1 2 3 4 5 6 7 8 Subclinical IBD Clinical IBD • Subclinical Gumboro: few clinical signs, strong immunosuppression. • Clinical Gumboro: more distinct clinical signs, immunosuppression.
  12. 12. Clinical Signs: -Sudden onset of self-vent picking with vent inflammation. -Depression & severe prostration due to serum calcium depletion. -Ruffled feathers with soiled vent feathers due to the copious watery yellowish white diarrhea leading to dehydration. -Anorexia, in-coordination, wobbly gait and trembling. The signs, morbidity & mortality are most evident in birds older than 3 wks of age. Mortality varies from 1-10% in commercial broilers & baby-chicks future breeders while in commercial layers & balady breeds it may be 30-50%. Mortality occurs in a characteristic spiking curve hence the mortality gradually increases through the 1st three to four days of the disease course then suddenly decline. The disease usually runs its course in 4-7 days, but outbreaks of 2-3 days are also possible.
  13. 13. Influencing factors Some factors which can influence the severity of a field infection: a) infection pressure. b) virus characteristics. c) level of immunity. d) genetic constitution. e) other immune-suppressive agents 2.3.a infection pressure: The IBDV is very stable and can survive for months on a farm even without birds. It's very resistant to several disinfectants. Consequently, once a farm is infected only extremely thorough cleaning and disinfection can reduce virus pressure, elimination of the virus will be extremely difficult. But with sound sanitary measurements and good vaccinations, the disease can be controlled.
  14. 14. 2.3.b virus characteristics: Most of the Gumboro isolates belong to the same serotype (serotype I) but there is a wide variety within this serotype. Both the pathogenic type and most of the weak types used for vaccination belong to this group. The serotype II isolates were first found in turkeys. This type can also infect chickens. 2.3.c genetic constitution: The genetic constitution of the bird influences the ability to respond to vaccines and to pathogenic field exposure. There appears to be a relation between the bursa size and the susceptibility to IBD. In general susceptibility occurs in the following order from greatest too lowest: white layers, brown layers and meat type birds. 2.3.d other immune-suppressive agents: Various agents, besides IBD viruses are known to give an immune-suppressive effect. The best known examples are Chicken Anemia Virus (CAV), Reticulo Endotheliosis Virus (REV) and Mycotoxines, which can effect the response to Gumboro challenge or vaccination.
  15. 15. 2.3.d level of immunity There are 2 forms of immunity; active and passive. Passive immunity consists of the maternal antibodies derived from the mother. Active immunity is a result of developed antibodies after challenge with field virus or after challenge with vaccine virus. The level of maternal immunity depends on the immune status of the parents; the vaccinations and the disease history influence this. These two together will greatly influence the optimal moment for vaccination. A vaccination for Gumboro can only be effective if the vaccine virus can break through the level of immunity of the chicken. Vaccine virus can be neutralized by maternal antibodies if they are at a high level, in this situation vaccination is done too early. When field virus will break through the maternal immunity it will lead to an immune-suppression. Birds, which have suffered from IBD, have a definitely lower response to vaccinations for example ND.
  16. 16. Days of Course Mortality % Spiking Curve Of Mortality Spiking
  17. 17. Chicks may be infected when only a few days old “sub-clinical IBD”. Although no clinical signs nor inflammatory bursal lesions are seen, permanent damage to the bird’s immune system occurs in birds up to 3 wks of age. 1-This predisposes the birds to other diseases known as “Gumboro- related diseases”. They are: -Gangrenous dermatitis & Ulcerative enteritis. -Inclusion-body hepatitis. -Coli-septicemia. -Coccidiosis. 2-It also reduces their response to the routine vaccination against other diseases e.g. ND, IB, coccidiosis and ILT.
  18. 18. PM Lesions
  19. 19. Enlarged bursa which may be covered with gelatinous material. This occurs in 3-5 days post-infection.
  20. 20. The interior of the bursa may be filled with gelatinous or caseous material.
  21. 21. Hemorrhagic or even blackish-brown bursa externally and internally. This occurs with more virulent classic strains of IBDV.
  22. 22. Bursal atrophy at the end of the coarse of the disease “ the 8th day PI”. This atrophy is due to lymphoid cell depletion.
  23. 23. Petecheal or ecchymotic hemorrhage on the lateral aspect of the thigh muscles and sometimes with congestion of the pectoral muscles.
  24. 24. Hemorrhage at the junction between the proventriculus and gizzard.
  25. 25. Enlargement of the proventricular wall. This may be due to the dual simultaneous effect between IBDV and Reo viruses
  26. 26. Swollen pale kidney due to deposits of urates. Some authors tend to denotes this kidneys as “wormy kidney”.
  27. 27. Histopathology
  28. 28. Immunosuppression IBDV attacks the rapidly proliferating “immature” lymphocytes in BF leading to severe lymhocytic apoptosis → severe suppression of humoral immunity whose persistence is dependent on the age of occurrence. •less severe & transient suppression of cell mediated immunity. incidence of other diseases, e.g. Marek’s, UE & GD, Coccidiosis. antibody response to standard vaccination program e.g. ND, IB. Chickens infected with IBDV at one day of age are completely devoid of serum immunoglobulin G (IgG) and produce only monomeric IgM.  non-specific morbidity and mortality.  performance.
  29. 29. Determining Percentage Bursa Weight It is the weighing of cleaned bursa in correlation to the whole body. If both the whole bird and the bursa are weighed, the bursa weight can be calculated as a percent of body weight: % Bursa Weight = (Bursa weight /Body Weight) x 100%. A 2000 g bird with a 4 g bursa, for example, would have 0.2% bursa weight. The bursa should be measured with a scale accurate to 0.1 g and the whole bird with one accurate to 20 g. Table-Rating % Bursa Weight in Broiler Flocks -Excellent = 0.30% and Over -Average = 0.18% to 0.20% -Questionable = 0.15% to 0.18% -Poor = Under 0.15%
  30. 30. Diagnosis Sub-clinical IBD A history of chicks with very low levels of MDA (Fewer than 80% positive in the immunodifusion test at day old, Elisa vaccination date prediction < 7 days), subsequent diagnosis of 'immunosuppression diseases' (especially inclusion body hepatitis and gangrenous dermatitis) is highly suggestive. This may be confirmed by demonstrating severe atrophy of the bursa, especially if present prior to 20 days of age. The normal weight of the bursa in broilers is about 0.3% of bodyweight, weights below 0.1% are highly suggestive. Other possible causes of early immunosuppression are severe mycotoxicosis and management problems leading to severe stress. 2-Laboratory diagnosis: -Direct Virus Isolation. -Indirect Serological Identification. -Histopathological examination.
  31. 31. Diagnosis of Clinical IBD 1-Field diagnosis -Case History. -Clinical signs. -Typical bursal gross lesions. 2-Laboratory diagnosis: -Direct Virus Isolation. -Indirect Serological Identification. -Histopathological examination.
  32. 32. Direct Viral Examination 1-Virus Isolation -Bursa in the acute stage is the best source for virus isolation due to the high viral concentration. -The virus is isolated by inoculation of CAM of chicken embryo (9- 11 days old). -The embryos die in 3-5 days post-inoculation showing mottled liver, kidneys and congested lung. -IBDV is also isolated in tissue culture of chick embryo fibroblast, embryo bursal cells and/or mammalian cell lines by serial passages. The inoculated virus may produce plaques in the inoculated tissue culture.
  33. 33. The liver appears pale, bile stained and with wide necrotic foci.
  34. 34. 2-Electron Microscopic Examination: Negative Shadow techniques of IBDV shows the virus particles with its characteristic viral morphology.
  35. 35. Indirect Serological Identification 1-Immunofluorescence: This is dependent on the examination of smears of cryostat sections of infected bursal tissues or inoculated embryo or cell culture stained with convalescent IBD infected birds or hyper-immunized rabbits serum conjugated with immunofluorescence reagent shows brilliant fluorescence in the bursal follicles on examination by fluorescence microscope.
  36. 36. 2-Agar gel precipitation test: *The collected bursal tissues from suspected clinical cases are taken and homogenized into 50% w/v suspension in PBS. The homogenate is centrifuged at 3000 rpm for 20 minutes & the supernatant is used as antigen. *The suspected antigen is placed into the central well of the AGP plate while the known sera are placed into the peripheral wells. *Incubate the plate into a bacteriological incubator at 37 C for 24 hrs in a humid atmosphere. *Positive test is obtained by the appearance of a precipitation line between the central well and the peripheral well containing a specific known antiserum.
  37. 37. 3-Enzyme linked immunosorbant assay (ELISA) Purified virus is coated on microtitre plates or commercial test kits are used. Usually a single serum dilution is used. The results of ELISA can be read on ELISA reader. In positive cases reddish brown color is seen. It is a good method for testing large number of samples.
  38. 38. 4-Specific diagnostic tests: -Antigen-capture ELISA: specific test depending on the monoclonal IBDV antibodies. -Virus neutralization test: The test of choice for diagnosis and measuring IBDV antibodies. -Polymerase chain reaction “PCR”: specific test depending on the detection and proliferation of IBDV using the thermocycler.
  39. 39. Immunity of IBD • MDA is the basic protective immunity during the critical first 2 wks of age. • Humeral antibody is the basic protective immunity, after the start of the vaccination program. • Cell-mediated immunity has a limited role.
  40. 40. Prevention of IBD Effective biosecurity program: Proper sanitary precautions are required to break the cycle of infection. Effective breeder IBD vaccination program: to attain a very good level of MDA passively transferred from the breeder hens to their progeny. MDA protects chicks from infection during the critical first 2 wks of life when IBDV may cause permanent immunosuppression. Effective broiler IBD vaccination program: Vaccination is the principal means of control according to the proper parameters.
  41. 41. Effective biosecurity program Proper sanitary precautions are required to break the cycle of infection. Proposal biosecurity program 1-Dry cleaning “proper removal and disposal of poultry litter as quickly as possible”. 2-Wet cleaning with liquid soap and water “20 liter liquid soap + 500 liter water” for cleaning of 1500 cubic meters. 3-Disinfection “20 liter of formalin + 3 liter of malathion + 500 liter of water” to disinfect of 1500 cubic meters - - - or - - - “2 kg Virkon S + 3 liter of malathion + 500 liter of water” to disinfect of 1500 cubic meters”. 4-Trafic control of workers, visitors and veterinarians. 5-Rodent and dog control.
  42. 42. Epidemiology Key factors in the epidemiology of IBDV: • The disease is highly contagious, spreading through the movement of poultry products, equipment, feed bags, vehicles and people, and, to a lesser extent, through aerosols of dust. • Clinical signs of the disease are age related, with birds 3–6 weeks most susceptible to clinical disease. • The antibody status of the exposed birds will influence the clinical expression of the disease. • The genotype of the birds affects clinical expression, with layer breeds being more susceptible. • The virus is highly resistant to heat and chemicals, and can persist in the shed environment for at least 4 months. • Normal shed cleaning practices may be inadequate to eliminate the virus. • Processed and frozen poultry meat may contain infectious virus. • The virus is not egg transmitted but can survive on the eggshell surface. • Natural infection is usually via the oral route, but the upper respiratory tract and conjunctiva (eye) probably also play a role. • The role of wild birds & rodents is uncertain, but they may act as mechanical carriers. • Mealworms (Alphitobius diaperinus) have been implicated as reservoirs, and Aedes vexans mosquitoes as vectors, of IBD virus. Mealworms are extremely difficult to eliminate from earthen-floored sheds. • Infected chickens continue to excrete the virus in their faeces for up to 2 weeks after infection.
  43. 43. 1.6.4 Factors influencing transmission The extent to which vvIBD or eavIBD may spread in Australia will largely dependon the: • location of the initial outbreak; • immune status of the flock; • time before detection; • efficiency of diagnosis of early cases; • number of contacts with the infected farm; • movement of poultry; • level of biosecurity being practised on farms in the region; • poultry density of the farm and region; and • (possible) wild bird and rodent movement from the infected farm.
  44. 44. Effective breeder IBD vaccination program This is to attain a very good level of MDA passively transferred from the breeder hens to their progeny. MDA protects chicks from infection during the critical first 2 wks of life when IBDV may cause permanent immunosuppression. Proposal breeder IBD vaccination program An example of a comprehensive breeder vaccination program have a vaccine schedule such as this: -At 12 days of age -- live intermediate IBD vaccine. -At 20 days of age -- live intermediate IBD vaccine. -At 30 days of age -- live intermediate IBD vaccine. -At 85 days of age -- live intermediate IBD vaccine or inactivated. -At 120 days of age --IBD inactivated. -Revaccinate at 38-42 wks of age with an inactivated IBD vaccine if breeder titers are low or of poor uniformity. Routinely monitor breeder IBD antibody titers to ensure vaccines are administered properly and that the chickens respond appropriately.
  45. 45. Effective broiler vaccination program Vaccination is the principal means of control according to the proper parameters for designing a vaccination program. Parameters for Designing IBD Vaccination program 1-Estimation of the quantity of MDA passively transferred from the breeder hens to their progeny depending on the “ELISA”. 2-Estimation of the uniformity of MDA passively transferred from the breeder hens to their progeny depending on the estimation of the “Coefficient of Variation = CV”. 3-Breed of birds to estimate the “Half life time of MDA”. 4-Epidemiological status of the geographic area to determine the “degree of IBD epidemiology”. 5-Aim of vaccination. 6-The used vaccine Strains → Cloned or non-cloned Mild, Intermediate or Intermediate plus Value of Mab of break through of each Vaccine type
  46. 46. 1-Quantity of MDA High LowModerate 2-Uniformity of MDA Coefficient of variation = CV. CV = SD/N x 100 -30% or less → strongly uniformed →1 vaccination. -30-50% → moderately uniformed → 2 vaccination. -50% or more → weakly or non-uniformed → 3-4 vaccination times. First vaccination timing depends upon various factors including status of MDA, type of bird, disease pressure and housing conditions. Vaccination frequency depends upon the degree of MDA uniformity.
  47. 47. Initial vaccination at 1 to 7 days followed by Booster vaccination “s”. Low, Non-Uniform, or Unknown MDA Levels Effect of Quantity & Uniformity of MDA High and Uniform MDA Levels Single vaccination at 10-14 days of age.
  48. 48. 1-In commercial broilers → 4 days. 2-In commercial layers & breeders → 5 days. 3-In Balady breeds & house holding birds → 6 days. 3-Breed of birds (Half life time of MDA). Epidemiological status of the geographic area.-4 Circulating strains Classic = virulent VariantVery virulent
  49. 49. 5-Aim of vaccination Ring = MetaphylaxisRoutine = Prophylaxis Vaccinal Strains-6 Cloned or non-cloned Value of Mab of break through of each Vaccine type Mild, Intermediate or Intermediate plus
  50. 50. Table: Vaccine strains of IBDV. VirulenceCloningStrainCompanyIBDV Strain Intermediate ClonedD-78IntervetNobilis D 78 Intermediate Non-clonedBursineFort DodgeBursine 2 Intermediate + = “hot' Non-cloned BursineFort DodgeBursine + Intermediate + = “hot' Non-cloned 2512MerialIBDV Blen IntermediateNon-cloned LuckertBiomune Co.Bursimune IntermediateNon-cloned S 706MerialGallivac S706 Intermediate ClonedMoulthropScheringBursa Vac 3 Intermediate + = “hot' ClonedMoulthropScheringBursa Vac plus
  51. 51. Proposal routine broiler IBD vaccination program An example of a comprehensive broiler routine vaccination program have a vaccine schedule such as this: -At 8 days of age -- live intermediate IBD vaccine. -At 13 days of age -- live intermediate IBD vaccine. -At 19 days of age -- live intermediate IBD vaccine. Ring “Metaphylaxis” broiler vaccination program Ring “Metaphylaxis” vaccination program If there is a production unit of multi-houses is stocked by chickens and one house is infected by IBD. Ring “Metaphylaxis” vaccination means the immediate vaccination of the other non-infected houses as soon as possible using one the cloned vaccines especially strain D-78 or Bursa vac-3.
  52. 52. 6.2.1. Live vaccines The objective of a live vaccination of broilers is to induce a protective level of immunity before a field virus can infect the bird. This is a difficult thing to accomplish because one needs to find the optimum date for vaccination. The average level and the variation (spreading) of the maternal immunity influence this. Another important factor is the strength of the vaccine used. There are mild, intermediate and hot vaccine strains. Vaccination is possible at the moment when the ELISA titers are 1:128 for intermediate vaccines and 1:512 for “hot” vaccines. The half-life time of maternal antibodies in broilers is 3- 3,5 days and for meat type breeders 4 days. The half-life time of maternal antibodies in layers is 4-5,5 days. Blood sampling must be done as soon as possible, but you must take into account that the half life time counting starts after 3 days. The first 3 days the yolk is used. Sometimes a double vaccination is needed when there is a relative big variation in the titers. Hot strains are used when very virulent IBDV is present.
  53. 53. 6.2.2 Inactivated vaccines Inactivated vaccines can be given to breeders in order to increase the level of maternal immunity in the offspring. Priming with a live vaccine should always precede it. World- wide there are 2 systems practiced for IBD priming. The cheapest method is only the priming used as first vaccination at +/- 21-24 days of age. Some producers use a second priming (live vaccine) at 6-14 weeks of age in order to try to get a higher and a more uniform titer at (Grand) Parent stock level. The killed vaccine can be given as a combination with other vaccinations. Some producers do not use inactivated IBD vaccines; this will lead to a higher variation in titers, especially when Parent stock is challenged with field virus.
  54. 54. Advises for vaccinating chickens against IBD. -Try to prevent mixing chickens derived from different parent stock flocks, with different levels of maternal immunity against IBD. -When given in the drinking water → a good quality cool drinking water and properly cleaned drinkers (no traces of disinfectants) is essential to avoid neutralization of the virus. Add 1% skimmed milk powder to the water to protect the virus (before opening the vaccine vials). Thirsten the birds for 2 hrs (summer) and 3 hrs (winter), then provide enough drinking water with vaccine for 1.5–2 hrs. To check the drinking water vaccination technique one can use water-soluble dyes. Other vaccination techniques can be used as eye drop vaccination method. Another vaccination method is in-ovo “inovation” technique. The vaccine is injected into the hatching eggs, at the transfer time “the 18th days of incubation”. Maternal antibody levels have no influence on this technique.
  55. 55. Control of IBD The specific treatment is not available up till now but from our practical experience we can try the followings: 1-Reduction of crude protein% of feed i.e. formulate a final feed with relatively high corn% and low soya bean% → to reduce the metabolic uric acid load on the kidney tissues. 2-Use of a multivitamin + immunostimulant “Immunair” supplement and facilitating access to water. 3-Use of diuretics “Renyl or Diurel” → 1 gm/liter/8hrs/3 days. 4-Spraying of Verkon-S solution in the atmosphere of the farm → 20 gm/10 liter water daily for 3 days. 5-Antibiotic medication may be indicated if secondary bacterial infection occurs .
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Dr Fares El-khayat -Infectious bursal disease

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