RESUMEN
The objective of this study was to analyze the in vitro antimicrobial resistance (AMR) of Streptococcusdysgalactiae, Strep. agalactiae, and Strep. canis over a 10-yr period from 2012 to 2022 against the most commonly used antimicrobial agents. For this purpose, all quarter milk samples (QMS) submitted to the milk laboratory of the Bavarian Animal Health Service were analyzed. Each QMS was tested using the California Mastitis Test and categorized as negative, subclinical, or clinical mastitis if the milk character was abnormal. Samples with Strep. dysgalactiae, Strep. agalactiae, or Strep. canis were included and a subset of isolates were further tested for in vitro AMR by breakpoint analysis with broth microdilution. Streptococcus dysgalactiae (61%, n = 65,750) was the most abundant pathogen among those 3 species, followed by Strep. agalactiae (28%, n = 30,486), and Strep. canis (11%, n = 11,336). All 3 species showed the highest resistance to the same 4 antimicrobial agents: erythromycin, marbofloxacin, pirlimycin, and cefalexin/kanamycin with varying degrees of resistance. Throughout the study period, Strep. dysgalactiae, Strep. agalactiae, and Strep. canis were largely susceptible to the remaining antimicrobial agents tested (penicillin, amoxicillin-clavulanate, oxacillin, cefazolin, cefoperazone, cefquinome). Only less than 14% of isolates of Strep. dysgalactiae and Strep. canis were resistant against any of the antimicrobials tested. Streptococcus agalactiae was the species with the highest percentage of resistant isolates. Although the percentage of resistant isolates from Strep. canis and Strep. dysgalactiae decreased, the percentage of resistant Strep. agalactiae isolates increased after 2017. In summary, most isolates were not resistant to the most commonly used antimicrobial agents for mastitis therapy, including ß-lactam antibiotics and penicillin should remain the first-choice therapy against streptococcal mastitis.
Asunto(s)
Antibacterianos , Mastitis Bovina , Leche , Infecciones Estreptocócicas , Streptococcus agalactiae , Streptococcus , Animales , Leche/microbiología , Streptococcus agalactiae/efectos de los fármacos , Streptococcus agalactiae/aislamiento & purificación , Streptococcus/efectos de los fármacos , Streptococcus/aislamiento & purificación , Alemania , Femenino , Bovinos , Mastitis Bovina/microbiología , Infecciones Estreptocócicas/veterinaria , Infecciones Estreptocócicas/microbiología , Antibacterianos/farmacología , Pruebas de Sensibilidad Microbiana , Antiinfecciosos/farmacología , Farmacorresistencia BacterianaRESUMEN
Pb(p, xn) thick target excitation functions were measured in the energy range 10-38 MeV in order to optimize the production of isotopically pure radiobismuth from natPb, 206Pb, and 207Pb. Additionally, the decay of Po-isotopes from deuteron irradiation of natural bismuth (209Bi) was exploited for radiobismuth production. 205Bi was produced from 206Pb at 20 MeV with only 2% of 206Bi at 4 weeks post irradiation. Bismuth compounds as used in the treatment of peptic ulcer were labeled with 205Bi for absorption studies in animals and subjects.
Asunto(s)
Bismuto/farmacocinética , Heces/química , Radioisótopos/farmacocinética , Bismuto/sangre , Bismuto/orina , Ciclotrones , Humanos , Proyectos Piloto , Radioisótopos/sangre , Radioisótopos/orinaRESUMEN
2-[18F]-FDG, a non-physiological glucose analogue, is the most important positron-emission- tomography (PET) radiopharmaceutical. As an example we refer to the production of 2-[18F]-FDG at the research center in Karlsruhe. 2-[18F]-FDG is synthesized in a "no carrier added" process. It is delivered at a maximal filling volume of 10 ml from a 14.5 ml batch with a batch-to-batch yield fluctuation from 5075 to 50,750 MBq and a specific activity from 1 to 10 GBq/mumol. The residual remaining synthesis reagents like solvents or catalysts have no toxicological relevance. The applicated dose per patient is in a range from 185 to 370 MBq and 1000 times lower than the correlating concentrations of stable FDG which can be regarded harmless in animals. 2-[18F]-FDG does not interfere with normal glucose metabolism. It is taken up by cells and phosphorylated to 2-[18F]-FDG-6-phosphate. The following dephosphorylation step is slow and the labeled compound is retained over several hours within the cells. Non-metabolized 2-[18F]-FDG is excreted rapidly in the urine to an extent of about 16% after 60 min, and 50% after 135 min, respectively. Fluorine-18F decays by emission of 511 KeV gamma photons. The whole body effective dose is reported to be 21 to 27 microSv/MBq. In case of an intravenous injection of 370 MBq this leads to a total dose of 7.8 to 10 mSv. The critical organ is the bladder wall (radiation dose 120 to 170 microSv/MBq or 80 to 100 mrem/mCi). The risk of a radiation induced late malignoma at 10 mSv can be estimated to be 1:2000. The genetical risk as a consequence of FDG-PET diagnostics would be 1:100,000 to 2:100,000 for dominant, and 5 times higher for recessive mutations.
Asunto(s)
Glucemia/metabolismo , Fluorodesoxiglucosa F18/efectos adversos , Tomografía Computarizada de Emisión , Humanos , Dosis de Radiación , Monitoreo de RadiaciónRESUMEN
Hematopoietic stem cell transplantation is characterized by a prolonged period of humoral immunodeficiency. We have previously shown that the deficiencies are probably not due to the failure to utilize the appropriate V regions in the pre-immune repertoire. However, a striking observation, which correlated with the absence of immunoglobulin IgD(-) cells and was consistent with a defect in antigen-driven responses, was that rearrangements in bone marrow transplant (BMT) recipients exhibited much less somatic mutation than did rearrangements obtained from healthy subjects. In this paper, we present evidence suggesting that naive B cells obtained from BMT recipients lack the capacity to accumulate somatic mutations in a T-cell-dependent manner compared with healthy subjects. This appears to be a B-cell-autonomous deficit because T cells from some patients, which were not able to support the accumulation of mutations in autologous naive B cells, were able to support accumulation of mutations in heterologous healthy-subject naive B cells.