Our technical group’s efforts in manu-facturing and research are achievingexcellent results. We have tripled our production capacity of Marek’s vaccineand other live vaccines since we beganthe company, and our success rate for serial release has shown incredibleimprovement.We cut the ribbon on the $4.5 millionexpansion of our new production facili-ties in June. Our objective is to increaseour inactivated capacity and to lower our costs, thereby increasing our competi-tiveness. Additionally, the facility’s GMPstatus will allow shipment of productinto the EU, another step in the expan-sion of our opportunities.To streamline and improve our productdistribution, we consolidated UnitedStates and Canadian distribution into our Gainesville, Ga., site. With multiple coldstorage facilities, computerized links toboth manufacturing sites and experiencedpersonnel, we can provide quick, efficientdelivery of vaccine to our customers inthis important market area. Both MBLand Vineland vaccines can be sourcedfrom this location by calling toll free800-655-1342 beginning July 1, 2001.Inventories, sent via refrigerated trucks toGainesville, will be on hand to supplyimmediate delivery requests.Now in the final stages of develop-ment, our new 30,000-square foot com-mercial, packaging and distribution cen-ter in Vineland, New Jersey, will be com-pleted and operating August 1, 2001.This new facility is geared to satisfy thespecific needs of our international cus-tomers. On-line labeling will allow for custom label requirements to be met near the time of order processing.To better serve our customers and sup-port our distributor partners, we dividedsales management of the Vineland,Maine Biological Laboratories andLohmann Animal Health brands in July.Under this structure, LAHI, based in theU.S., serves North, Central and SouthAmerica, and LAH, based in Germany,serves the rest of the world. Each manu-facturing center will continue to supplytechnical and registration informationabout their specific products, but day-to-day sales and marketing will correspondwith geographical lines.We are proud of these efforts, showcasing what a dedicated group of peoplecan accomplish with the proper resources.Our success translates into excellent sup-ply and service for our global customer base, encompassing poultry professionalsin more than 56 countries.
ALOHMANN ANIMALHEALTH INTERNATIONALNEWS BRIEF
Infectious Bursal Disease Virus:AContinually Moving Target
Joseph J. GiambroneProfessor of Poultry Science Auburn University, Auburn, Al 36849-5416 firstname.lastname@example.org:/www.auburn.edu/~giambjj/
Infectious bursal disease (IBD), oftenreferred to as bursal or Gumboro disease,has been a constant thorn in the side of the commercial chicken industry since itsdiscovery in Gumboro, Delaware, in thelate 1950s. In the 1960s and
70s, thishighly contagious viral disease mainlyappeared in the clinical form, affectingchickens between two and four weeks of age. Affected birds (about 30% of theflock) were pale, ruffled-up, lethargic,had an unsteady gait, and white or red-dish diarrhea. Mortality was moderate(20% or less) and weight gain and feedefficiency were poor.
The virus was resistant to most disinfec-tantsat the time and, therefore, was con-trolled through the use of fairly virulentlive vaccines consisting of groundhomogenates from the bursa of Fabriciusof chickens infected with field isolates.The bursa is the tiny lymphoid organ inthe hindgut of all birds, and is the targetorgan for replication of the virus, whichcauses the disease. These homogenateswere given to 1- to 2-week-old chickensby drinking water. This would result in amild form of the disease with about 5%mortality and 10% morbidity. Developedin the southern United States, this formof controlled exposure, otherwise knownas
fighting fire with fire,
would againcome to the forefront 25 years later inEurope for the control of very virulentIBD virus (V). Nevertheless, these fairlyvirulent vaccines given to very youngchickens significantly reduced the clini-cal form of disease seen prior to their usein the field.
In the 1980s came the milder, embryoand cell culture derived vaccines. Theseproducts were much safer than previousvaccines and were widely used through-out the world. Although these virusesadequately controlled the clinical form of IBDV, a new, previously unrecognizedform appeared. The virus was found toproduce atrophy of the bursa of Fabriciusand immunosuppression, when chickenswere infected with the virus during thefirst few weeks of age. This form did notcause clinical disease, and, therefore, wasknown as the subclinical immunosup-pressive form. This form decreased theimmune response of infected chickens tosubsequent vaccination and increasedtheir susceptibility to pathogenic organ-isms in the field. Affected flocks wouldhave a higher incidence of respiratory,enteric, and integumentary diseases.These flocks often had much higher pro-cessing plant condemnations resulting inconsiderable economic losses. The controlof this subclinical immunosuppressiveform required the use of a combination of live and newly developed inactivatedvaccines in the breeder pullet flocks.These hyperimmunized hens then passedhigh and uniform amounts of maternalantibody to their progeny. This passiveimmunity would protect the chicks for the first two to three weeks of age.
With the widespread use of live andkilled vaccines in the parent flocks, thespread of highly concentrated and inten-sive chicken populations, and the use of rearing flocks on built-up litter, a major change occurred in the IBDV
s molecular structure.New antigenic variants first appearedin Delmarva Peninsula in the late 1980sand then spread throughout the world inthe 1990s. These viruses underwent achange in the structure of the VP2 gene,which helped them survive in the poultryindustry, where vaccination was common.This gene codes for the major viral capsidprotein, which induces neutralizing anti-body in the infected chicken. Asmallsegment of this gene, less than 120nucleic acid base pairs in length, iswhere the important variation occurred.Only one base alteration in the right areacaused a change in a critical amino acid.This change altered the binding site of the virus for the antibody, epitope, whichbestowed on the virus the ability toescape neutralization by antibody. Thisgenetic site in the VP2 is known as thehypervariable region. These variant
In this issue of avian insight:
Infectious Bursal Disease Virus......................
From the President............
continued on page 2
Dave Zacek,President of Lohmann Animal Health International,Gainesville,Georgia,USA
from the president…
a v i a n i n s i g h t
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