O slideshow foi denunciado.
Seu SlideShare está sendo baixado. ×

Gumboro Disease

Mais Conteúdo rRelacionado

Audiolivros relacionados

Gratuito durante 30 dias do Scribd

Ver tudo

Gumboro Disease

  1. 1. Dr .Omnia Ebrahim
  2. 2.  Infectious bursal disease also known as IBD, Gumboro Disease, Infectious Bursitis and Infectious Avian Nephrosis  a highly contagious disease of young chickens caused by IBDV . characterized by immunosuppression and mortality generally at 3 to 6 weeks of age.  The virus attacks the birds lymphoid organs especially the bursa were it affects the B-cells causing immunosuppression. Let’s just say the bird’s immune system is affected and it becomes susceptible to all sorts of infections.  Affected chickens have reduced antibody response to vaccinations, strong post vaccinal reactions, and increased susceptibility to concurrent or secondary infections.
  3. 3.  Clinical disease is associated to bird age with the greatest bursal mass, which occurs between 3 and 6 weeks of age. The greatest bursal mass is mostly a result of a large population of maturing IgM-bearing B- lymphocytes (lymphoblasts), the main target of infection. Young birds at around two to eight weeks of age that have highly active bursa of Fabricius are more susceptible to disease. Birds over eight weeks are resistant to challenge and will not show clinical signs unless infected by highly virulent strains.  The bursa of Fabricius, which is the organ responsible for disease protection in young birds, is the main target for the virus. Normally, the bursa of Fabricius regresses by early maturity. Hence, infectious bursal disease is most important in birds up to 4 week of age, and most critical between 2 and 4 weeks of age.  Subclinical disease occurs in chickens infected before three weeks of age. At this age the B-lymphoblast population is smaller and the systemic effects are insufficient for generating clinical signs.
  4. 4.  IBD was first described as a specific new disease by Cosgrove in 1962 in the town of Gumboro, Delaware, USA.  Variant IBDV strains were first reported in the USA in 1986/87.  Hyper or very virulent IBDV strains were first reported in Belgium and The Netherlands in 1987.  Currently IBDV has a worldwide distribution, occurring in all major poultry producing areas.  The classical and hyper virulent forms of IBD are predominant in all countries with the exception of North America and Australia.  In the USA the variant strains of IBDV predominate
  5. 5.  During embryonic development, and through approximately 10 weeks of age, immune system cells (lymphocytes) travel to the BF to become programmed to become antibody-producing cells. If the IBD virus damages the BF in young chickens, the BF will not be capable of programming sufficient numbers of lymphocytes. Thus, the chickens will experience reduced immune system capabilities (immunosuppression).  After ingestion, the virus destroys the lymphoid follicles in the bursa of Fabricius as well as the circulating B-cells in the secondary lymphoid tissues such as GALT (gut-associated lymphoid tissue), CALT (conjuntiva), BALT (Bronchial) caecal tonsils, Harderian gland, etc. Acute disease and death is due to the necrotizing effect of these viruses on the host tissues. Kidney failure is a common cause of mortality. If the bird survives and recovers from this phase of the disease, it remains immunocompromised which means it is more susceptible to other diseases.
  6. 6.  Morbidity rate very high reaches to 100 %  Mortality rate in borilers 20 – 30 % and in layers and Baladi 50-70%  Immunosuppresion which leads to the birds are susceptible to 2ry infections such as NDV , IB , HVT ,Inclusion Body Hepatitis and gangrenous dermatitis and increased susceptibility to CRD.
  7. 7.  IBDV is a double stranded RNA virus .  belongs to the genus Avibirnavirus of family Birnaviridae .  There are two distinct serotypes of the virus, but only serotype 1 viruses cause disease in poultry.
  8. 8.  Five viral proteins desighnated : VP1 , VP2 , VP3 , VP4 , VP5 have been recognized.  VP1 plays a key role in the encapsidation of the virus particle.  VP2 encodes the major antigenic determinants of the virus, including epitopes that are important in virus neutralization.  VP3 is a group specific antigen that is recognized by non-neutralizing antibodies. VP3 acts as an intermediary, interacting with both VP1 and VP2, and the formation of VP1-VP3 complexes is likely to be an important step in the morphogenesis of IBDV particles.  VP4 is a minor and non-structural polypeptide.  VP5 likely has a regulatory function.
  9. 9. Virus Classification: IBDV strains are classified into two distinct serotypes, differentiated by a virus neutralization test. There is no crossprotection between these serotypes. Serotype 1 Standard/Classic Antigenic Variants Pathogenicity • Mild • Classical • Very virulent • Vv.Virulent Immunosuppressant Serotype 2 a pathogenic infects ducks and turkeys but does not cause clinical disease or immunosuppression.
  10. 10. 1.Mild field and vaccine IBDV strains: cause no mortality or clinical symptoms, but bursal damage dependant on virulence of the virus may still be evident. 2.Classical IBDV strains: cause mortality (<20%) and bursal lesions. Able to break through a moderate level of maternal derived antibody. 3.Hyper or very virulent IBDV strains: cause severe mortality (>20%) and bursal lesions. Able to break through higher levels of antibody than classical strains.
  11. 11.  Via Ingestion ( horizontally through contaminated food and water )  Mechanical transmission via people , animals ,vehicles and equipments when transferred from diseased flock to healthy one .  May be via the conjunctiva or respiratory tract, with an incubation period of 2-3 days.  It has been demonstrated that the lesser mealworm (Alphitobius diaperinus) could act as a vector carrying IBDV from one cycle to the next.  There is no vertical transmission. (no transmission from parent to day old chick through the egg)  The virus remains after previous history of disease for 122 days .  The infected birds shed virus for 14 days n their feces. Feed, water, and poultry house litter become contaminated.
  12. 12.  Due to the hardy nature of the virus it persists in the environment of the poultry house, infections are thus potentially carried over from one cycle to the next.  he virus is resistant to many disinfectants such as :  QACs 1000ppm , also resistant to 0.5 % formalin for 5 hours .  PH 2  60ْ C for 30 minutes and 56ْ C for 1 hour in prescense of 0.5 % phenol .
  13. 13.  Effective disinfectants :  0.5 % cholramine  0.5 % NaOH  Iodine 50 ppm  PH 12  80ْ c FOR 10 minutes .
  14. 14.  Infectious bursal disease follows one of two courses, depending on the age at which chickens , breed and virulence of field virus  1-clinical form  2-subclinical form
  15. 15.  The clinical form of IBD usually occurs in chickens from 3 to 6 weeks of age .  appears in : sudden onset of mortality rate and poor performance  1-a rapid drop in feed and water consumption  2- mucoid (slimy) diarrhea with soiling of the vent feathers  3- depression,ruffled feathers and closed eyes  4- Many birds may be reluctant to move with a tendency to sit  5-picking at own vent and sleeping with beak touching the floor  6-poor FCR so variability in body weight .  7-Affected chickens experience a transient immunosuppression.
  16. 16.  Age of birds  presence or absence of passive immunity.  Mangment ( cleanout and Disinfection )  Breed  Virulence of field virus  concentration of IBD  Exposure time
  17. 17.  The subclinical form of the disease occurs in chickens less than 3 weeks of age. Chickens present no clinical signs of disease, but experience permanent and severe immunosuppresion  Early subclinical infections are the most important form of the disease because of economic losses. The disease can cause severe, long-lasting suppression of the immune system. Chickens immunosuppressed by early IBDV infections do not respond well to vaccination and are predisposed to infections with normally nonpathogenic viruses and bacteria.
  18. 18.  Very virulent (vv) strains of the virus that cause high mortality and morbidity were detected first in Europe.
  19. 19.  Oedematous bursa (may be slightly enlarged, normal size or reduced in size depending on the stage), may have haemorrhages, rapidly proceeds to atrophy. Five days after infection, the BF diminishes in size rapidly .  Haemorrhages in skeletal muscle (especially on thighs) and junction of the proventriculus and gizzard.  . because the IBD virus interferes with the normal blood clotting mechanism.  Swollen kidneys with urates. Such lesions probably result form severe dehydration, not direct viral damage.  Dehydration.  Chickens that have recovered from IBDV infections have small, atrophied, cloacal bursas due to the destruction and lack of regeneration of the bursal follicles.
  20. 20. Gumboro disease: Summary of expected changes in bursal size, weight and morphology Days post infection Size Morphology 2 - 3 Bursa increases in size and weight  Oedematous with gelatinous yellow transudate covering serosal surface.  Color changes from normal white to a cream color.  Petechial to extensive haemorrhaging may be present. 4 Bursa double the normal weight and size 5 Bursa returns to normal weight Transudate and edema disappear. Bursa turns a grey color.8 Bursa 1/3 of original weight
  21. 21. Variant IBDV strains do not cause as severe an inflammatory response. However severe bursal atrophy is characteristic and mortality is usually less than 5%. Very virulent IBDV strains cause severe lesions in other lymphoid organs such as the thymus, caecal tonsils and spleen in addition to bursal lesions. with high mortality. Normal bursa and atrophied bursa post IBDV infection
  22. 22. Bursas from Left to Right: 1) Acute stage. Enlarged edematous bursa 2) 5 days post infection bursa returns to normal size. May be hemorrhagic as in this specific bursa 3) 8 days post infection bursa atrophied and up to 1/3 of normal size 1 2 3
  23. 23. Bursa from inside with petechial hemorrhages. Hemorrhages at the juncture of proventriculus& gizzard. petechial hemorrhages present in pectoral muscles
  24. 24.  Microscopically, lymphocyte necrosis is present in the BF within 36 hours after infection. By 48 hours, few lymphocytes are present. Edema, hyperemia, and inflammatory cell infiltration are evident.  By 8 to 12 days after infections, the BF is shrunken to less than one- fourth of its original size. The lymphoid follicles are cystic and depleted of lymphocytes. The epithelium lining the BF is irregular and infolded. Fibroplasia is present in the interfollicular connective tissue.
  25. 25. Histopathology slide of healthy bursa Histopathology section of atrophied bursa in severe cases of IBD, all the follicles are affected simultaneously. In less severe cases, only scattered follicles are affected, and the lesions spread to other follicles. Typically, the follicles in the tips of bursal folds are affected first.
  26. 26.  1-flock history  2-symptoms (Subclinical disease - A history of chicks with very low levels of maternal antibody (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. )  3-postmortem examination  4-histopathology  5- virus isolation and identification  6- Serology and fluorescent antibody techniques  7- RT-PCR (as mentioned above) was designed for the detection of IBDV genome  8- Serological tests such as agar gel precipitation and ELISA, for detecting antibodies
  27. 27.  Differentiate clinical disease from: Infectious bronchitis (renal); Cryptosporidiosis of the bursa (rare); Coccidiosis; Haemorrhagic syndrome.
  28. 28. IBDV COCCIDIOSIS 1- sudden onset 2-droopy appearance 3-ruffled feather 4-muscular hemorrhagic 5-enlarged edematous or hemorrhagic cloacal bursa 4-blood in dropping 1-Coccidiosis IBDV Avian Nephritis virus 1- Birds show kidney lesions &nephrosis 2-Cloacal bursal lesion &atrophy of bursa 2-NO clinical signs until 28 day of infection 2-disease cause nephrosis:
  29. 29.  There is no treatment for Gumboro virus , but support therapies, such as vitamin and electrolyte supplements and antibiotics to treat any secondary bacterial infections, may reduce the impact of the disease.  If secondary diseases become a problem, antibiotic therapy may be required, but this should be kept to a minimum.  Drug therapy is often inadvisable in the presence of severe kidney damage.
  30. 30.  Can be achieved by good mangment and suitable vaccination programme  An effective IBD prevention and control program must involve an effective breeder vaccination program, an effective biosecurity program, and an effective broiler vaccination program
  31. 31.  Good ventilation, warm temperatures and fresh water will help to reduce mortality.  All infected litter and carcases of infected birds must be suitably disposed of away from the site or any other poultry operation.  A thorough well planned disinfection regimen  -shift for cleanout  -followed by GPC 8 as an efficient disinfectant .  Downtime between successive flocks must be maximised. (A minimum of 10 days is recommended between successive broiler flocks.)  Control of the traffic ( people,vehicles and equipments )
  32. 32.  Vaccines need to be selected based on the types of viruses present in the area.  The timing of broiler vaccination depends on the level of maternal antibody present in the chicks. High levels of maternal antibody at the time of vaccination will neutralize the vaccine virus. Thus, only a limited active immune response results and chickens will be susceptible to disease as maternal titers decrease. If low levels of maternal IBD titers are present in the chicks, vaccination may not be effective on farms contaminated with virulent field virus. Basically, this means that vaccinating the chicks too early and too late will produce a negative effect and will not protect the birds.
  33. 33.  Three categories of vaccines, based on their pathogenicity, have been described:  1) mild  2) intermediate  3) intermediate plus (hot strain )  The intermediate type IBD vaccines are most commonly used. These vaccines can stimulate the broiler to produce antibodies earlier than the mild-type vaccines, without significant damage to the BF as may occur with the virulent type vaccines.
  34. 34.  Breeder flocks should be vaccinated one or more times during the growing period, first with a live vaccine and again just before egg production with an oil-adjuvanted, inactivated vaccine. Inactivated vaccines of chicken embryo. The immune status of breeder flocks should be monitored periodically with a quantitative serologic test such as virus neutralization or ELISA. If antibody levels fall, hens should be revaccinated to maintain adequate immunity in the progeny.
  35. 35.  Often IBD is a serious problem in an integration, and losses occur despite persistent efforts at reducing field virus exposure through a biosecurity program, maintenance of adequate and uniform maternal titers, and an effective broiler vaccination program. In this case, consideration should be given to vaccinating breeders with inactivated vaccines containing standard and variant strains of the IBD virus.
  36. 36.  1- Bursine 2 ( intermediate strain )  2- Bursine plus ( intermediate plus strain )

×