The objective of this study was to analyse the occurrence of methicillin-resistant Staphylococcus aureus (MRSA) in three dairy herds in the southwest of Germany that had experienced individual cases of clinical and subclinical mastitis associated with MRSA. The herds were identified by the detection of MRSA during routine resistance testing of mastitis pathogens. All quarters of all cows in the herds that were positive on California Mastitis Test were sampled for bacteriological analysis on two occasions. Bulk tank milk samples were also tested. Furthermore, nasal swabs were collected from people working on the farms and from cattle. Environmental samples were collected from associated pig holdings. Isolates were characterized using spa-typing and testing for antimicrobial resistance. Our results revealed a substantial spread of MRSA in the three dairy herds. In the first of the two investigations carried out on all cows in the three herds, milk samples of 5.1-16.7% of dairy cows were found positive for MRSA. The respective proportions in the second herd level investigation were 1.4-10.0%. Quarters harbouring MRSA had higher somatic cell counts than quarters that were negative on culture. Methicillin-resistant Staphylococcus aureus were also detected in nasal swabs of staff (7/9), cows (7/15) and calves (4/7), bulk tank milk samples (3/3) and environmental samples from pig premises (4/5) on the farm. Herds B and C had no contact to herd A. However, in all three herds MRSA of spa-type t011 were detected in milk samples. Results show that MRSA of spa-type t011 is a problem in dairy farms that needs urgent attention.

A total of 144 clinical isolates of Acinetobacter species, i.e., A. baumannii (n = 60), genospecies 3 (n = 48), A. haemolyticus (n = 12), and genospecies 6 (n = 24), were examined comparatively with the agar dilution method of the National Committee for Clinical Laboratory Standards for susceptibility to 25 antimicrobial drugs. Only minor species differences were noted.

Summary. A retrospective multicentre clinicopathological study was performed on sequential bone marrow trephine biopsies in 100 patients with Ph 1 -chronic myelogenous leukaemia (CML) to elucidate the effect of interferon (IFN) a 2b and hydroxyurea (HU) treatment on myelo®brosis and megakaryopoiesis. According to strictly de®ned therapeutic regimens, 38 patients received IFN as monotherapy, 23 patients a combination of IFN and HU and 39 patients HU only. Using standardized intervals of biopsies and histochemical and morphometric methods, a signi®cant increase in reticulin ®bre density and in the number of CD61 megakaryocytes was detectable in the majority of IFN-treated patients. To a lesser degree, these changes were also expressed in the cohort with a combined IFN and HU regimen. In contrast to these ®ndings, in the group of patients with HU as single-agent treatment, a stable state or reversal of myelo®brosis was detectable together with corresponding changes in megakaryopoiesis. Further evaluations revealed that these effects had occurred within the ®rst year, mostly after 6 months of treatment, and were prominently expressed in those patients with a slight to relevant grade of myelo®brosis at presentation. In conclusion, this study provides persuasive evidence that monotherapy by IFN exerts a ®brogenic effect, while HU treatment seems to prevent and even resolves bone marrow ®brosis in CML. Probably, in relation to the complex pathomechanisms responsible for the generation of myelo®brosis, the changing content of reticulin ®bres was usually accompanied by corresponding alterations in the number of CD61 megakaryocytes, including atypical microforms and precursor cells.

Twelve clinical isolates of Pseudomonas aeruginosa of distinct pyocin type varied in susceptibility to 14 of 17 antimicrobial drugs. The 2 x MIC concentrations of 16 antimicrobial drugs combined with 55% (v/v) of fresh, defibrinated human blood yielded additive effects. Additive effects were noted with blood plus the MIC concentrations of all drugs tested except cefoperazone, gentamicin, and netilmicin. Blood combined with subinhibitory (1/2 MIC) concentrations of aztreonam, ceftazidime, ciprofloxacin, fleroxacin, imipenem, and tobramycin, respectively, yielded additive effects; indifferent effects were observed with the remaining 10 blood plus 1/2 MIC drug combinations. The following drug combinations additively augmented the antibacterial activity of 65% (v/v) of human blood against two selected isolates of P. aeruginosa: tobramycin (1 μg/ml) plus the MIC or 2 x MIC concentrations of azlocillin, aztreonam, ceftazidime, ciprofloxacin, imipenem, norfloxacin, ofloxacin, piperacillin, and ticarcil-lin, respectively. Imipenem (8 μg/ml) combined with ceftazidime, cefoperazone, and piperacillin, but not aztreonam, enhanced the bactericidal activity of human blood. Rifampin (2 μg/ml) plus tobramycin (0.5–1 μg/ml) combined with 8 or 16 μg/ml of azlocillin, aztreonam, cefoperazone, ceftazidime, imipenem, and piperacillin, respectively, enhanced blood-mediated killing of three representative multiple-drug-resistant P. aeruginosa isolates. Additional effective triple-drug combinations with human blood were rifampin + tobramycin + polymyxin B, rifampin + ciprofloxacin + imipenem, and rifampin + amikacin + imipenem. Ciprofloxacin (2 μg/ml) was the most potent intra-phagocytic bactericidal drug of 16 tested agents ( ≥ 2 x MBC concentrations) against P. aeruginosa control strain ATCC 27853.

Ampicillin, fusidic acid, gentamicin, imipenem, mezlocillin, ofloxacin, penicillin G, piperacillin, and vancomycin were examined for inhibitory and bactericidal activity in various broth media against 7 clinical isolates of Streptococcus faecalis. On a weight-for-weight basis, ampicillin, imipenem, mezlocillin, and ofloxacin proved to be more efficacious. All enterococcal isolates were resistant against gentamicin; fusidic acid and vancomycin lacked bactericidal activity. The combinations of either ampicillin, imipenem, mezlocillin, ofloxacin, piperacillin, or vancomycin with a subinhibitory concentration (4 μg/ml) of gentamicin, with or without added 65% (v/v) fresh defibrinated human blood, respectively, yielded additive effects against all enterococcal isolates. The addition of fresh human blood failed to enhance the antienterococcal activity of 4 μg/ml of gentamicin; in contrast, addition of 65% (v/v) fresh or heat-inactivated (56°C, 30 min) normal rabbit, bovine, and human sera augmented the activity of gentamicin, an effect that was ablated through the addition of either 0.005 M DTT or 0.01 M MgCl₂ + 0.01 M EGTA + 0.01 M CaCl₂, supplements known to antagonize human serum β-lysin, but not lysozyme activity.