Catabolic pathways of glucose in Bacillus circulans var. alkalophilus.

Enzymes and the metabolic pathways of glucose catabolism of Bacillus circulans var. alkalophilus were studied. The metabolism of the microbe was mixed acid fermentative yielding mainly acetic and formic acids as end products from glucose. It was estimated that B. circulans var. alkalophilus partitions 90%-93% of the carbon from glucose into the Embden-Meyerhof-Parnas (EMP) pathway and 7%-10% into the hexose monophosphate (HMP) and Entner-Doudoroff (ED) pathways. Rather low activities of glucose dehydrogenase and gluconokinase appeared in the early logarithmic and late stationary phases, whereas NADH oxidase was markedly high. This result can be explained by a demand to reduce NADH to NAD+ for the EMP pathway; when acetic and formic acids are produced, no NADH is regenerated to NAD+, which is required in the early steps of EMP and HMP pathways. A small percentage (1.6%-2.4%) of the total CO2 was formed from (6-C) of glucose, which means that the tricarboxylic acid cycle was functional but its contribution was insignificant. Large differences do not seem to exist between alkaliphilic and neutrophilic bacilli in the use of glucose pathways.

Haemolytic-uraemic syndrome caused by vero toxin-producing Escherichia coli serotype Rough: K-: H49.

The first case of haemolytic-uraemic syndrome (HUS) caused by Vero toxin-producing Escherichia coli (VTEC) which belonged to a novel serotype, Rough: K-: H49, is reported. The case was initially diagnosed as nephropathia epidemica caused by Puumala virus, but the subsequent diagnosis of HUS caused by VTEC was made after bacteriological investigation. The strain isolated fermented sorbitol produced VT2 toxin but not enterohaemolysin, nor did it carry the eaeA gene. In VTEC strains, the O antigen, the eaeA gene and enterohaemolysin production have been characterized as virulence-associated factors and believed to have an effect on pathogenesis of these strains to cause haemorrhagic colitis or HUS. The findings of this study demonstrate that there is a need for further studies to evaluate the pathogenetic mechanism of VTEC and need for easy diagnostic methods exploiting other properties than O157 antigen and non-fermentation of sorbitol to find all VTEC in human infections.

Swimming-associated outbreak of Escherichia coli O157:H7.

In 1997 the first outbreak of Escherichia coli O157:H7 infections involving 14 cases occurred in Finland. A case was defined as a resident of Alavus with an episode of diarrhoea between 5 and 17 July 1997, and from whom E. coli O157:H7 was isolated from stool. The investigation included case searching and a population-based case control study. Five primary and eight symptomatic secondary cases of E. coli O157:H7 illness were detected. In the 10 days before the outbreak, all 5 primary patients (aged 3-8 years), but only 6 of 32 population controls from the same age range (Fisher's test, P < 0.001) and 4 of 10 sibling controls (P < 0.05) had visited (but had not necessarily bathed in) a shallow beach popular among young children. Four out of 5 primary cases had remained within 5 m of the beach while swimming and had swallowed lake water compared to 1 of 5 population controls. These analytical epidemiologic findings incriminated fresh lake water as the vehicle of E. coli O157:H7 transmission.

Development of beta-lactamase-mediated resistance to penicillin in middle-ear isolates of Moraxella catarrhalis in Finnish children, 1978-1993.

The frequency of beta-lactamase production was analyzed in a study of 1,452 strains of Moraxella catarrhalis and 2,738 strains of Haemophilus influenzae isolated from middle-ear fluid of children < 6 years of age at Tampere University Hospital in Tampere, Finland, between 1978 and 1993. In addition, 401 isolates of M. catarrhalis from similar samples collected in different parts of Finland in 1988-1990 were tested for beta-lactamase production; minimal inhibitory concentrations of ampicillin, cefaclor, cephalothin, erythromycin, tetracycline, and trimethoprim-sulfamethoxazole for these strains were determined. These data were compared with figures for the annual consumption of beta-lactam antimicrobials in the community in 1978-1993. A bimodal increase in the proportion of strains of M. catarrhalis producing beta-lactamase was detected: from 0 to 60% in 1978-1983 and from 60% to 80% in 1988-1990. Concurrently with the second increase, the consumption of cephalosporins increased substantially in the community. The frequency of beta-lactamase-producing strains of H. influenzae did not increase between 1978 and 1993.

Antimicrobial resistance of Streptococcus pneumoniae in Finland, 1987-1990.

A nationwide survey of the prevalence of antimicrobial resistance among Streptococcus pneumoniae isolates from the middle ear fluid of children with acute otitis media (639 strains) and from throat-swab samples of healthy children (149 strains) was conducted in Finland during 1987-1990. The MICs of penicillin, cephalothin, cefaclor, erythromycin, trimethoprim, and co-trimoxazole were determined by the agar dilution method. Low-level resistance to penicillin (MIC, 0.1-1 microgram/mL) was found in 1.7% of the otitis-related and 1.3% of the healthy-carrier strains. No highly penicillin-resistant strains (MIC, > or = 2 micrograms/mL) were found. Six multiresistant strains were detected, three of them possibly belonging to a previously identified clone present in Finland since 1985. Eighty-five percent of the resistant otitis-related strains, including 9 of the 11 moderately penicillin-resistant strains (4 of which were multiresistant), belonged to the three most common serogroups (6, 19, and 23).

Antimicrobial resistance in Haemophilus influenzae isolated from blood, cerebrospinal fluid, middle ear fluid and throat samples of children. A nationwide study in Finland in 1988-1990.

A nation-wide survey of the prevalence of antimicrobial resistance in Haemophilus influenzae was conducted on isolates collected in 1988-90 from middle ear fluid (MEF), blood, or cerebrospinal fluid (CSF) in infected children or throat samples of healthy children. Altogether 885 strains were examined regarding capsular type b, beta-lactamase production and the minimal inhibitory concentration (MIC) of ampicillin, cefaclor, erythromycin, tetracycline, chloramphenicol, trimethoprim and trimethoprim-sulfamethoxazole for these strains was determined by the agar dilution method. 99% (578/585) of MEF isolates, 93% (112/121) of throat isolates, but only 6% (10/179) of blood/CSF isolates were not of type b (Hib). The rate of beta-lactamase production was 11.4% among Hib strains, 8.0% among non-type b MEF isolates, and 4.5% among non-type b throat isolates. No increase in the prevalence of beta-lactamase production in H. influenzae has taken place in Finland since the early 1980s. Resistance to ampicillin among strains that lacked beta-lactamase activity was rare (0.2%). Of the non-type b MEF and throat isolates, 5.9% and 2.7%, respectively, were resistant to trimethoprim and 3.6% and 2.7%, respectively, to trimethoprim-sulfamethoxazole. Resistance to other drugs was rare (< 2%) in all isolate groups.