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The frequency of beta-lactam resistance was determined among 313 strains of Escherichia coli, 119 of Enterobacter/Klebsiella/Proteus spp., and 48 of Pseudomonas spp. isolated from blood cultures (at Turku University Central Hospital and Turku City Hospital) in 1983-1987. During this period the MIC50 of ampicillin for Escherichia coli increased from 8 to 32 µg/ml, the MIC90 of piperacillin from 16 to > 32 µg/ml and the MIC90 of cefuroxime from 4-8 to 16 µg/ml. Among 172 ampicillin-resistant isolates beta-lactamase-mediated resistance was characterized by DNA hybridization with TEM-1, SHV-1, OXA-1, OXA-2, PSE-1, PSE-2 and PSE-4 beta-lactamase probes and by isoelectric focusing. Beta-lactamase types found were TEM-1, TEM-2, SHV-1 and OXA-1. Isoelectric focusing did not show any other plasmid-mediated beta-lactamase varieties. Piperacillin-resistant strains showed mostly TEM-1 activity, but also produced OXA-1 and chromosomal beta-lactamase. Interestingly, a decrease in cefuroxime susceptibility in Escherichia coli occurred in a few OXA-1 producing strains as well as in strains that produced only chromosomal beta-lactamase. Two Escherichia coli strains that overproduced chromosomal beta-lactamase had increased ceftazidime MIC values (8-16 µg/ml). [ABSTRACT FROM AUTHOR]

Antimicrobial resistance of faecal aerobic Gram-negative bacteria to eight different antimicrobials was determined by a velvet replica-plating method in 1988 and 1933. Faecal samples were taken from 131 geriatric inpatients in the Turku City Hospital with a hospitalization of more than 7 days. From 1987 to 1992 the use of first and second generation cephalosporins and ciprofloxacin increased from 3.32 defined daily doses (DDD) per bed to 24.25 DDD/bed and from 0.63 DDD/Bed to 28.11 DDD/bed, respectively. A statistically significant increase was observed in the frequency of samples resistant (with >= 1% of resistant colonies) to cefuroxime (p = 0.0004) and ceftazidime (p = 0.037) in patients who received antimicrobial therapy and to ampicillin (p = 0.046) in patients who had not received antimicrobial therapy. In addition, despite the decreased use of sulphonamides and trimethoprim (from 17.11 DDD/bed to 5.54 DDD/bed) no significant changes in the frequency of resistant faecal samples were observed. Use of ciprofloxacin has been found to cure resistance plasmids from bacteria in vitro. However, despite the increased use of ciprofloxacin, no decrease in faecal bacteria resistant to any of the other antimicrobials (i.e. trimethoprim) studied was observed. [ABSTRACT FROM AUTHOR]

From 1983 to 1989, 520 Escherichia coli blood culture pathogens were isolated from two hospitals in Turku, Finland. Ampicillin resistance (MIC≥16 µg/ml) of these isolates increased from 33 % in 1983 to 66 % in 1987, but decreased to 38-49 % in 1988-1989. Occurrence of TEM-1 beta-lactamase producing isolates increased only slightly from 14 % in 1983 to 25 % in 1989 among all Escherichia coli strains studied. Strains with ampicillin MIC values of 16 µg/ml and 32 µg/ml were mostly responsible for the increase in resistance. Among these isolates, TEM-1 or any other of the well known plasmid-mediated beta-lactamases were not found by hybridization or isoelectric focusing. [ABSTRACT FROM AUTHOR]

Limb girdle muscular dystrophies are a large group of both dominantly and recessively inherited muscle diseases. Dominantly inherited LGMD1 diseases are usually milder and later onset forms than recessive LGMD2. We have followed six Finnish families with LGMD1D and reported clinical and MRI findings in these families. All families represent the same DNAJB6 mutation, causing a F93L change in the ubiquitously expressed co-chaperone DNAJB6. The molecular pathogenesis of LGMD1D is mediated by defective chaperonal function leading to impaired handling of misfolded proteins which normally, without the defect, would be degraded and re-cycled. We have analyzeded 14 muscle biopsies obtained from 13 patients in six families at very different time points after onset of muscle weakness symptoms. All biopsies were from lower limb muscles, either vastus lateralis or gastrocnemius medialis and processed for routine histology, histochemistry as well as extensive immunohistochemistry and semithin sections with subsequent electron microscopy. Uniform findings were myopathic/dystrophic changes in all patients. Restricted and easily overlooked myofibrillar pathology in routine histopathology included protein aggregates reactive for Z-disk proteins such as myotilin, desmin and alphaB-crystallin was a regular finding in the early stages of pathology. These formed Z-disk alterations, streaming and dispersion of Z-disk material on the ultrastructural level. Later in the disease process the pathology was dominated by rimmed vacuolar pathology. These were reactive for several markers of defect autophagy such as ubiquitin, TDP-43, p62 and SMI-31. Since DNAJB6 is known to interact with members of the chaperone assisted autophagy complex (CASA), including BAG3 – a known myofibrillar myopathy causing gene, the molecular muscle pathology is apparently mediated through impaired functions of CASA and eventually other protein complexes needed for the maintenance of sarcomeric and Z-disk structures. [Copyright &y& Elsevier]

The susceptibility of 455 Escherichia coli blood culture isolate to piperacillin was tested with the disk diffusion test. The presence of different beta-lactamase genes in these strains was also studied using DNA hybridization. Of the TEM beta-lactamase producing isolates, 64 % (61/95) were interpreted as intermediately susceptible to piperacillin. Because piperacillin is hydrolyzed by TEM-type beta-lactamases, we suggest that the intermediate susceptibility category should be reduced or omitted in testing piperacillin susceptibility of Escherichia coli isolates. [ABSTRACT FROM AUTHOR]