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R Meir

Publications and source records attributed to R Meir.

22 records · Page 2Linked to original sources

Molecular typing of infectious bursal disease virus of Israeli field and vaccine strains by the reverse transcription/polymerase chain reaction/restriction fragment length polymorphism assay.

Infectious bursal disease viruses (IBDVs) were examined by testing bursa samples from 37 commercially reared chicken flocks and three vaccine strains by the reverse transcription (RT)/polymerase chain reaction (PCR)/restriction fragment length polymorphism assay (RFLP). The assay was conducted with a 717-bp fragment of the VP2 gene with the restriction enzymes BstNI and MboI. The presence of a restriction site for SspI was used to predict a very virulent phenotype. Results indicated the existence of two molecular groups within the field isolates; four samples showed one pattern of RFLPs, and the majority, 30 out of the 37 tested, showed a second RFLP pattern. Three samples tested negative for IBDV. Eight bursa samples, representing the two molecular groups, were also tested by the RT/PCR/RFLP assay as developed by Jackwood. A comparison of the RFLP profiles by the two methods indicated that four isolates belonged to molecular group 6 and 30 isolates belonged to a new molecular group. All field isolates had a very virulent phenotype. One vaccine strain, produced from a local isolate, was classified as molecular group 6. The other two vaccine strains had RFLPs that differed from those of the field isolates.

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Applications of the polymerase chain reaction to detect infectious bursal disease virus in naturally infected chickens.

Reverse transcriptase-polymerase chain reaction was used for identification of Israeli isolates of infectious bursal disease virus (IBDV). The system was applied to tissue culture and to bursa of Fabricius from infected chickens; these latter samples had been frozen for as long as 4 years. From base homology analysis of published sequences of serotype 1 IBDV, two pairs of primers, targeted to amplify sequences from the VP2 and VP3 cistrons, were prepared. The two sets of primers could detect viruses of serotype 1. The primers directed to the cistrons could detect viral sequences from seven infected chickens. No reaction was detected with RNA extracted from bursal cells of healthy chickens or from uninfected cells. The sensitivity of the reaction was equivalent to 2.5 x 10(1) TCID50.

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Causes of losses including a Borna disease paralytic syndrome affecting young ostriches of one breeding organization over a five-year period (1989-1993).

Necropsy records and causes of mortality of ostriches up to 3 months old over a 5-year period (1989-1993) are presented. The data relate to one ostrich enterprise that comprises 10 breeding flocks, five rearing farms, and one hatchery. Causes of mortality are classified into nine major categories. The annual mortality percentages of all hatched ostriches over the 5-year period were 61%, 58%, 30%, 29%, and 16.6%, and the most significant cause of death was a paresis syndrome that accounted for 20%, 11%, 16%, 10.1%, and 2% mortality, respectively. Limb deformities and gastroenteritis were the other principal specific causes of mortality. The paresis syndrome was caused by an agent serologically related to Borna disease virus. Brain extracts from paralyzed ostriches, when given orally or intramuscularly to 5-week-old birds, reproduced the clinical signs and microscopic lesions. The mean time to death was less than 3 weeks for the intramuscularly infected group and was almost twice as long for the orally infected group.

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