Biomedical subjects
J Bryner
Publications and source records attributed to J Bryner.
Antibody response of dairy cattle experimentally infected with Listeria monocytogenes.
The purpose of our study was to monitor the humoral immune response of 34 lactating dairy cattle experimentally infected with Listeria monocytogenes (strain Scott A, serotype 4b). Twenty-seven animals were inoculated with 10(6) to 10(7) c.f.u./ml of L. monocytogenes via the intramammary route at ten day intervals for one month and 7 were inoculated with 4 x 10(2) to 4 x 10(3) c.f.u./ml. Preinfection and weekly-post infection serum and whey samples were prepared during acute infection. Antibody titres of serum and whey were evaluated in agglutination tests using whole-cell formalin-fixed L. monocytogenes suspensions. Preinfection agglutination titres ranged from 1:20 to 1:320. At least four-dilution increase over pre-infection titres were apparent by the 8th week of infection. Eighty per cent of the bovine sera (26/34) exhibited titres of greater than or equal to 1:20, 480. Whey titres, which reflected the local humoral response to L. monocytogenes, rarely exceeded 1:256 which may be ascribed in part to the lower immunoglobulin concentration in milk vs. blood. Antibody levels indicate active listeriosis but could not be used to predict the magnitude of the recovery of Listeria (c.f.u./ml) in milk.
Research on listeriosis in milk cows with intramammary inoculation of Listeria monocytogenes.
The purpose of our work was to produce 600 litre quantities of milk containing (per ml) 5000 viable Listeria monocytogenes, for certification of standard pasteurization technique. Preliminary research indicates deep (10 cm) inoculation via teat canal with 3 injections, (10(3), 10(5), 10(7)) per 10-day interval, was better than intraocular or per os route for establishing chronic L. monocytogenes mastitis. Although milk yield diminished 25%, chronic L. monocytogenes shedding persisted for 8 months. Sheeding in individual cows varied from 10(3) to 10(5) listeriae/ml. Dexamethasone injections increased L. monocytogenes shedding in milk ca. 1000-fold. Three of 30 cows were pregnant during the experiment and produced normal calves, indicating that intramammary L. monocytogenes infection was localized and did not migrate to the pregnant uterus. Four of 30 cows developed CNS symptoms of listeriosis, and one died. From 11 cows, L. monocytogenes was isolated at necropsy, from mammary tissues (9/11), supramammary lymph nodes (9/11), liver (6/11), spleen (5/11), and brain (6/11) by cold enrichment culture. Serum antibody titres of infected cows increased from 1: 160 to 1: 10,280 in most cows. Large scale pasteurization trials led to the conclusion that the present pasteurization guidelines of the FDA are adequate to inactivate listeriae in whole milk.
Prepartum changes of plasma concentrations of prostaglandin F and 13,14-dihydro-15-ketoprostaglandin metabolites in pregnant animals exposed to Sarcocystis cruzi or Campylobacter fetus.
Pregnant cows at 4- to 5-months' of gestation were exposed to Sarcocystis cruzi or Campylobacter fetus. Plasma prostaglandin F (PGF) and 13,14-dihydro-15-ketoprostaglandin metabolite (PGM) concentrations were determined at intervals from before exposure until abortion or parturition. The plasma PGF concentration of pregnant infected cattle remained at 0.02 +/- 0.04 ng/ml until 24 to 48 hours before abortion or parturition when it increased 5-fold to 0.11 +/- 0.12 ng/ml. The plasma PGM concentration of these cattle remained at 0.10 +/- 0.07 ng/ml until 24 to 48 hours before abortion or parturition when it increased over 10-fold to 1.36 +/- 0.60 ng/ml. This change in PGF and PGM was similar to that of cattle exposed to each of the infective agents and to that of normal cows at parturition. Thus, changes in PGF and PGM concentrations in bovine plasma cannot be used as a diagnostic tool to determine fetal distress or fetal death for these infections.
Dynamic hormonal tests in a case of premature ovarian failure.
The case of a patient with premature ovarian failure and a history of polycystic ovarian disease was described. Dynamic gonadal and pituitary tests were done. Ovarian, adrenal, and peripheral veins were catheterized to determine the steroid secretion under HCG stimulation. In vitro studies of the capacity of ovarian steroidogenesis confirmed the refractory nature of the gonad. Lack of gonadal response, both in vivo and in vitro, to stimulation suggests a possible alteration in ovarian sensitivity to gonadotropins as a possible cause of premature menopause.