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B De Groot

Publications and source records attributed to B De Groot.

5 recordsLinked to original sources
PubMed1997

Effect of booster vaccination with a multivalent clostridial bacterin-toxoid on sudden death syndrome mortality rate among feedlot cattle.

OBJECTIVE: To determine whether booster vaccination with a multivalent clostridial bacterin-toxoid would affect the sudden death syndrome (SDS) mortality rate among feedlot cattle. DESIGN: Field trial. ANIMALS: 83, 115 cattle at a Nebraska feedlot. PROCEDURE: Cattle arriving at the feedlot underwent routine processing according to established protocol. All cattle received a sequentially numbered ear tag and a 2-ml dose of a multivalent bacterin-toxoid designed to protect cattle against Clostridium chauvoei, C speticum, C novyi, C sordellii, and C perfringens types C and D. Approximately 90 days prior to slaughter, growth promotants were implanted in all cattle, and cattle were allocated to a treatment or control group on the basis of the last digits of their ear tag numbers. Cattle in the treatment group received a second 2-ml dose of clostridial bacterintoxoid; control cattle did not. RESULTS: Significant differences between groups in regard to crude, feeding pen, or SDS mortality rates were not detected. Sudden death syndrome mortality rate across both groups was 0.24%. If the SDS mortality rate in midwestern feedlot cattle was reduced > or = 40% by booster vaccination with a multivalent clostridial bacterin-toxoid, this experiment included enough animals to have a 90% probability of detecting that difference. CLINICAL IMPLICATIONS: Booster vaccination with a multivalent clostridial bacterin-toxoid does not affect SDS mortality rate among feedlot cattle.

Animals↗
PubMed1980

Participation of bacteriophage T4 gene 41 in replication repair.

The location of the non-essential T4 mutant uvs79, with defective replication repair, is described. After crosses with double mutants dispersed over the early region of T4, a linkage was observed with the double mutant am41 : am42. For more accurate location, crosses were made with single mutants. Uvs79 proved to be located between mutants amC23 and amN81 in gene 41, as shown by 3-point crosses. No genetic complementation with respect to multiplicity reactivation was found between amN81 and uvs79 after co-infection of an su- host. Apparently, mutant amN81 is disturbed as to replication repair and, owing to its lack of DNA synthesis, also in replication-dependent recombination repair. Consequently, the product of gene 41 has a function additional to its RNA-primer induction during replication of undamaged DNA. Presumably, the product of gene 41 induces RNA primers opposite DNA regions containing lesions. This capability is believed to be specifically affected by the uvs79 mutation.

Crosses, Genetic↗