Biomedical subjects
Publications and source records attributed to K Roos.
A total of 21 erythromycin-resistant strains were found among 355 (5.9%) beta-hemolytic streptococci group A isolated in Göteborg during spring of 1987. T-typing showed 17 to be T12, 1 T4 and 3 nontypable. Spread of resistant strains could be demonstrated within 2 families and 1 day-care-center. Monitoring of erythromycin resistance among beta-hemolytic streptococci is advocated.
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Proteinase activity has been demonstrated in middle ear effusions from patients suffering from otitis media with effusion. Proteinase activity was characterized by various biochemical, chemical and physical parameters. Chelators and sulfhydryl group reacting substances reduced the enzyme activity. Enzyme activity was positively correlated to the number of granulocytes present in the effusion. No correlation to bacteriological findings or to tympanic membrane status was seen and the proteinase activity showed wide ranges within different categories of middle ear effusions.
Beta-streptococci isolated from patients with acute tonsillitis were tested for penicillin tolerance defined as an MBC/MIC ratio greater than or equal to 16. 11/18 strains recovered from patients with clinical treatment failure were tolerant to penicillin in comparison with 0/15 strains from successfully treated patients. The MBC/MIC ratio was less than 16 for all strains versus cefadroxil but above that ratio for many strains versus clindamycin, doxycycline and erythromycin. We suggest that penicillin tolerance may be one reason to treatment failures in individuals with streptococcal tonsillitis and that other antibiotics could be used to treat these patients since penicillin tolerance is not correlated to a general increase in antibiotic resistance.
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The pharmacokinetics of phenoxymethylpenicillin in tonsillar tissue was studied in 33 patients who underwent tonsillectomy, mainly because of repeated tonsillitis or peritonsillitis. The patients were operated on 30-240 min after an oral penicillin dose of 12.5 mg/kg body weight. The mean serum concentration was 2.8 micrograms/ml for 10 patients operated upon 80-95 min after drug administration. The mean tissue concentration for these patients at the same time was 0.6 micrograms/g. The mean concentration of penicillin in tissue after 240 min was 0.05 micrograms/g. 19% of the serum concentration was recovered in the tonsillar tissue. No significant difference between penicillin concentration in the centre or surface of the tonsils was found. The tissue concentration was calculated to be above 0.03 micrograms/ml for at least 4-5 h. 30% of the patients harboured penicillinase producing bacteria on their tonsils, mainly Staphylococcus aureus. These patients had a lower tissue concentration than those lacking the bacteria, but the difference was not statistically significant (p = 0.095).
Out of 169 patients with streptococcal tonsillitis treated with phenoxymethylpenicillin, 13 (8%) developed a new clinical infection with the same streptococcal strain within 2 weeks of completing the therapy (clinical treatment failure) and 24 (14%) were clinically healthy but harboured the same streptococcal strain after treatment (bacterial treatment failure). Patients with clinical treatment failure showed beta-lactamase activity in their saliva pellet significantly more often than patients with bacterial treatment failure, healed streptococcal tonsillitis or non-streptococcal tonsillitis as well as healthy controls. In an interference study, clinical treatment failures were compared with healthy streptococcal carriers, i.e. persons living in the same household and harbouring the same beta-streptococcal strain. 11/12 healthy carriers had alpha-streptococci with interfering activity against their own beta-streptococcal strain, while the corresponding figure for the clinical treatment failures was 2/13. Furthermore, 6/12 healthy carriers had beta-streptococci inhibiting their own alpha-strains, while the streptococci in 11/13 clinical treatment failures had this ability. The beta-lactamase activity and the interference between alpha- and beta-streptococci may be a contributory cause to treatment failure in streptococcal tonsillitis.
The refractory period and the killing rate of beta-haemolytic streptococci after exposure to phenoxymethylpenicillin were tested in an in-vivo model. beta-Haemolytic streptococci were injected into steel net chambers implanted subcutaneously on the backs of rabbits. The rabbits were treated with infusions of phenoxymethylpenicillin, either as a single dose to measure the refractory period or as repeated doses in order to measure the killing rate of streptococci. The peak concentration of phenoxymethylpenicillin in tissue chamber fluid occurred about 16-120 min post infusion, and reached 0.4 mg/l in infected and 0.6 mg/l in uninfected tissue cage fluid. In the tissue cage fluid the phenoxymethylpenicillin concentration exceeded 0.03 mg/l, the MIC-value for the streptococcal strain used, for at least 6 h. After a single infusion there was a decline in viable count. The bacteria did not reach their original numbers until 60-70 h later. After the sixth infusion streptococci were no longer detectable in tissue cage fluid. There was a close correlation between viable counts before treatment and the time required for eradication of bacteria. L-phase variants of beta-haemolytic streptococci were not found when tissue cage fluid was plated on special media.
13/169 outpatients (8%) with streptococcal tonsillitis developed a new tonsillitis with the same strain within 2 weeks of completion of therapy (clinical treatment failures) and 24 (14%) remained carriers (bacterial treatment failures) after treatment with phenoxymethylpenicillin (penicillin V) 12.5 mg/kg body weight twice daily for 10 days. The mean serum concentration 60 min after penicillin V administration was 7.84 micrograms/ml. Very large individual differences in serum concentration were found but these differences could not be correlated to treatment failure. About 60% of the patients showed salivary concentrations around 0.03 micrograms/ml. Three strains of streptococci (groups C and G) from patients with bacterial treatment failure had MIC values of 0.06 and 0.12 micrograms/ml. A majority of the patients with clinical treatment failures had contact with individuals with high carrier rates of beta-hemolytic streptococci. It therefore seems likely that some so-called treatment failures in reality are new infections. In clinical treatment failures group A streptococci were twice as common as groups C + G. In bacteriological treatment failures the ratio between A and C + G was 1:1. Patients with nonstreptococcal tonsillitis as well as carriers of groups C and G may appear among bacterial treatment failures.
267 outpatients with acute tonsillitis were studied with regard to clinical signs and symptoms and presence of beta-hemolytic streptococci. Beta-hemolytic streptococci were found in 169 patients (63%), compared to 6/64 healthy controls (9%). Of the tonsillitis patients with beta-hemolytic streptococci, 80% harboured group A and 20% groups C and G. Five out of 6 controls had group C and G streptococci. Eight clinical signs and symptoms of acute tonsillitis were rated on a 10-point scale. A correlation was found between redness in the oropharynx and on the tonsils and positive culture for beta-hemolytic streptococci group A. The total WBC count, polymorphonuclear leucocytes and ratio of polymorphonuclear to mononuclear leucocytes were strongly correlated to a positive culture for streptococci group A. Groups C and G did not show these correlations. The study stresses the importance of quantitative culture technique and the value of this for diagnosis in the acute ill patient with tonsillitis.
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The interference between alpha-streptococcal strains obtained from patients with repeated tonsillitis and a collection of group A streptococcal strains were studied. For this purpose three in vitro methods were designed and compared. The results obtained by a simple plating technique suitable for screening purposes were found to correlate well with those using more laborious techniques. In a limited scale some of the alpha- and beta-streptococcal combinations were tested under in vivo conditions using a tissue cage model allowing repeated sampling. In most instances agreement between the results of the in vitro and in vivo methods was registered. Several alpha-strains having inhibitory capacity to the majority of a collection of group A streptococci belonging to different serotypes were found, but also alpha-strains with an inhibitory activity restricted to few group A isolates within a certain serotype. Also beta-streptococcal strains with growth inhibiting activity towards some alpha-strains were found. As the methods were chosen to eliminate many of the unspecific inhibitory factors and the beta-hemolytic test strains showed a pattern of inhibition that varied for each of the reference alpha-strains the activity is most likely attributed to bacteriocin-like substances.
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Investigation of an outbreak of contamination of dialysis drainage fluid with Acinetobacter calcoaceticus var. anitratus identified a previously unrecognized source for dialysis associated infections. Over a 4-month period, 25 peritoneal dialysis treatments were administered to 13 hospital patients. Of the 25 treatments for which culture results were available, 14 were associated with dialysis drainage fluid cultures positive for A. calcoaceticus. A water bath used to warm bottles of peritoneal dialysate before use was the reservoir for the bacteria, and investigation showed in vitro that bath water could contaminate the dialysate. It appears likely that the dialysate became contaminated when the prong of the fluid administration set was inserted through the rubber bung on the dialysate bottles. This outbreak illustrates the potential importance of environmental reservoirs in infections complicating peritoneal dialysis.
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