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A Bauernfeind

Publications and source records attributed to A Bauernfeind.

At least 55 records · Page 3Linked to original sources

PBP binding and periplasmic concentration as determinants of the antibacterial activities of three new oral cephalosporins in Escherichia coli.

The antibacterial activities of cefetamet, cefixime and cefuroxime were investigated in Escherichia coli with regard to their penetration rates through the outer membrane and their affinities for PBPs in Escherichia coli. The permeability coefficient of cefetamet was measured in E. coli C600 carrying a pUC18 plasmid derivative, in which the gene of a transferable cephamycinase (CMY-2) was cloned, whereas diffusion of cefixime and cefuroxime was measured in E. coli C600 harbouring the OXA-1 beta-lactamase gene. It was found that cefetamet penetrated 5 and 9 times faster than cefixime and cefuroxime, respectively. The correlation between antibacterial activities and PBP affinities was studied in E. coli C600 not producing beta-lactamases. In this strain, cefetamet and cefixime shared the same inhibitory activity (MIC = 1 microgram/ml for both antibiotics) and the same affinity for PBP 3 (ID50 = 0.25 micrograms/ml). Cefuroxime had a lower inhibitory activity (MIC = 4 micrograms/ml) and a lower affinity for PBP 3 (ID50 = 0.5 microgram/ml). Cefixime and cefuroxime had 20 and 10 times higher affinity, respectively, than cefetamet for PBP 1s. It was concluded that the superior PBP affinity of cefixime can counterbalance the better penetration of cefetamet through the outer membrane, whilst differences in either permeability or PBP affinity seem sufficient to explain the lower antibacterial activity of cefuroxime compared to cefixime, which might well be related to the poor stability of the cefuroxime molecule.

Bacterial Proteins↗

Comparative in-vitro activities of the new quinolone, Bay y 3118, and ciprofloxacin, sparfloxacin, tosufloxacin, CI-960 and CI-990.

The in-vitro activity of the new quinolone, Bay y 3118, was compared with that of ciprofloxacin, tosufloxacin, sparfloxacin, CI-960 and CI-990 against 1640 isolates belonging to 117 bacterial species. Against members of the Enterobacteriaceae, Bay y 3118 was as active as CI-960 and CI-990, up to four-fold more active than ciprofloxacin and tosufloxacin and up to 16-fold more active than sparfloxacin. The majority of Enterobacteriaceae which were resistant to ciprofloxacin (MICs > or = 2 mg/L) were sensitive to Bay y 3118. With the exception of ciprofloxacin which was less active, the activities of Bay y 3118 and the other comparator compounds were similar against Acinetobacter baumannii, Acinetobacter genospecies 3 and Acinetobacter strain 84. Bay y 3118 inhibited Pseudomonas aeruginosa isolates at concentrations comparable with those of ciprofloxacin. However, non-aeruginosa Pseudomonas spp. were four times more susceptible to Bay y 3118 than to ciprofloxacin. All of the agents tested were equally active against Haemophilus, Moraxella, Neisseria and Bordetella spp. Against staphylococci, Bay y 3118 was the most active compound, followed jointly by CI-990, sparfloxacin, CI-960 and tosufloxacin, and then ciprofloxacin. Bay y 3118 remained highly active against Staphylococcus aureus strains resistant to ciprofloxacin; the MIC90 (0.5 mg/L) was 16-fold less than that of CI-990 and sparfloxacin, 32-fold less than that of CI-960 and 128-fold less than that of tosufloxacin and ciprofloxacin. Against haemolytic and non-haemolytic streptococci and Enterococcus faecalis, Bay y 3118 was two- to 16-fold more active than the other compounds. It had only moderate activity against Listeria spp., but this was superior to that of all the other compounds tested. Bay y 3118 was also the most active agent overall against anaerobic bacteria, although CI-960 and CI-990 had slightly better activity against Gardnerella vaginalis. It inhibited Mycobacterium spp. other than Mycobacterium tuberculosis (Mycobacterium kansasii, Mycobacterium scrofulaceum, Mycobacterium gordonae, Mycobacterium xenopi, Mycobacterium flavescens, Mycobacterium avium and Mycobacterium fortuitum) at concentrations < or = 0.06-4 mg/L and was between two- and 128-fold more active than the other compounds against these isolates; the two strains each of Mycobacterium terrae and Mycobacterium nonchromogenicum were resistant to Bay y 3118. In this study, Bay y 3118 was shown to be the most active and most broad-spectrum of the new quinolone and naphthyridine derivatives.

Anti-Infective Agents↗

In-vitro activity of dirithromycin in comparison with other new and established macrolides.

Improvements with regard to the in-vitro activity of new macrolides are marginal and apply mainly to Haemophilus spp., Moraxella catarrhalis and Neisseria gonorrhoeae (e.g. azithromycin is two to eight times more active than erythromycin) and to non-enterococcal streptococci (e.g. clarithromycin is two to four times more active than erythromycin). The increase in activity against staphylococci is even less striking, being restricted to a few species and limited to clarithromycin (twice as active as erythromycin). The Enterobacteriaceae, as well as glucose non-fermenting Gram-negative bacilli, remain outside the therapeutic range of the new macrolides, as they were for the established compounds. The majority of enterococci and Corynebacterium jeikeium are resistant to all macrolides, whereas Corynebacterium diphtheriae is highly susceptible. In-vitro susceptibilities both of Campylobacter jejuni/coli and Helicobacter pylori indicate only moderate susceptibility to macrolides and the azalide. In the case of anaerobic organisms, clarithromycin is the most active macrolide against the majority of species. Dirithromycin, clarithromycin, roxithromycin and josamycin, and the azalide azithromycin, are similar in their antibacterial spectrum to erythromycin. New macrolides differ from established compounds largely in their pharmacokinetic behaviour and only minor progress has been achieved in improving their antibacterial spectrum.

Anti-Bacterial Agents↗

Bactericidal activity of antibiotics alone and in combination against Enterococcus faecalis in a pharmacodynamic model.

We evaluated the bactericidal kinetics of teicoplanin, mezlocillin, netilmicin, and ciprofloxacin alone and in dual combinations against strains of Enterococcus faecalis susceptible or resistant to ampicillin in a pharmacodynamic model reproducing in bacterial culture in active human plasma or Mueller-Hinton broth the serum kinetics of these antibiotics in humans. Killing was not different in cultures grown in plasma and those grown in broth. Antibiotics used alone had no or low bactericidal activity except for high-dose ciprofloxacin (600 mg intravenously [iv] twice daily or 750 mg orally twice daily), which achieved a 3- to 4-log reduction in colony-forming units (cfu). Netilmicin was equally active at 6 mg/kg once a day or 2 mg/kg three times daily in all combinations. No major increase in bactericidal activity was detected in any combination that included mezlocillin. Maximal synergistic killing was observed for the combination of teicoplanin plus netilmicin (both at three-times daily and once-daily dosing), which sterilized the bacterial cultures (initial inoculum, 10(6) cfu/mL). Combinations of ciprofloxacin at 600 mg iv twice daily and 750 mg orally twice daily plus either teicoplanin or netilmicin were less synergistic but equally effective in total killing as a result of the high bactericidal activity of ciprofloxacin alone.

Anti-Bacterial Agents↗

RU 29 246, the active compound of the cephalosporin-prodrug-ester HR 916. I. Antibacterial activity in vitro.

The aminothiazolyl-cephalosporin RU 29 246 is the active metabolite of the prodrug-pivaloyl-oxyethyl-ester HR 916. RU 29 246 in vitro activity includes a wide range of clinically relevant bacterial pathogens. Against methicillin-sensitive Staphylococci RU 29 246 (MIC90 of 0.25 approximately 2 micrograms/ml) was clearly more active than cefaclor, cefuroxime, cefpodoxime, cefixime and ceftibuten, but slightly less active than cefdinir. RU 29 246 inhibited hemolytic Streptococci of the serogroups A, B, C and G as well as penicillin-sensitive Streptococcus pneumoniae at concentrations similar to cefdinir, cefpodoxime and cefuroxime (MIC90 less than or equal to 0.13 micrograms/ml), but less than the other oral cephalosporins investigated (cefixime, cefaclor and ceftibuten). MIC90s of RU 29 246 against Escherichia coli, Klebsiella pneumoniae, Klebsiella oxytoca, Salmonella spp., Shigella spp., Proteus mirabilis and Haemophilus influenzae were less than or equal to 0.5 micrograms/ml. Only RU 29 246 and cefdinir demonstrated moderate activity against Acinetobacter baumannii (MIC90 greater than or equal to 4 micrograms/ml). Most strains of Pseudomonas spp., Serratia marcescens, Enterobacter spp., Hafnia alvei and Bacteroides spp. were resistant to RU 29 246. RU 29 246 killed Escherichia coli and Staphylococcus aureus at a rate of 99% to 99.9% at concentrations of two times MIC. The pH value of the medium (range 5.5 to 8.5) and the inoculum size (range 10(5) to 10(7) cfu/ml) had no or only low influence on the antibacterial activity of RU 29 246. RU 29 246 is a broad spectrum cephalosporin including in its activity both Gram-positive and Gram-negative pathogens and therefore--depending on the bioavailability of its prodrug--looks promising as to its therapeutic perspective.

Anti-Bacterial Agents↗

RU 29 246, the active compound of the cephalosporin-prodrug-ester HR 916. II. Stability to beta-lactamases and affinity for penicillin-binding proteins.

The aminothiazolyl-cephalosporin RU 29 246, the active metabolite of the prodrug-ester HR 916, is active against strains producing the widespread plasmid-encoded TEM-1, TEM-2 and SHV-1 beta-lactamases. Except for TEM-7 the activity of RU 29 246 against strains producing extended broad spectrum beta-lactamases (TEM-3, TEM-5, TEM-6, SHV-2, SHV-4, SHV-5, CMY-1, CTX-M), however, is low. Relative hydrolysis rates of RU 29 246 are comparable with those of cefpodoxime, the active metabolite of CS-807, and are extremely low for the TEM-1 and SHV-1 beta-lactamases. The compound demonstrates remarkable inhibitory activity against the chromosomal beta-lactamase of Enterobacter cloacae P99. In the presence of 1.7 microM this enzyme loses 50% of its activity. At concentrations of 0.43, 0.003 and 0.01 micrograms/ml the compound binds preferentially to the penicillin-binding protein (PBP) 3 of Escherichia coli K12, to the PBPs 2x and 3 of Streptococcus pneumoniae R6 and to PBP 1 of Staphylococcus aureus SG 511, respectively.

Anti-Bacterial Agents↗

[Outbreak of a nosocomial infection of SHV2-beta-lactamase-containing Klebsiella pneumonia strains in an operative intensive care unit].

Resistant strains of Klebsiella pneumoniae were found in increasing frequency as a cause of nosocomial infection in an intensive care unit between July and October 1990. The isolated strains had an almost identical biochemical profile, showed a similar pattern of antibiotic resistance, and produced type SHV2-broad-spectrum betalactamase. Thus, it was assumed that the isolates were copies of identical strains, causing an outbreak of nosocomial infections. The bacteria were resistant to third-generation cephalosporins, such as cefotiam, cefotaxime and ceftriaxone, and also to aminoglycosides and acylaminopenicillins. Approximately half of the strains were resistant to ceftazidim and aztreonam. The bacteria were sensitive in vitro to ciprofloxacin, imipenem, latamoxef and cefotetan. During three months, 10% (11) of all patients became infected; four of these patients (36%) died from septicemia. After conventional hygiene programs had failed to stop the outbreak, the intensive care unit was closed and disinfected, a measure, which effectively interrupted the infection.

Cephalosporins↗

In vitro activity and stability against novel beta-lactamases of investigational beta-lactams (cefepime, cefpirome, flomoxef, SCE2787 and piperacillin plus tazobactam) in comparison with established compounds (cefotaxime, latamoxef and piperacillin).

The therapeutic perspectives of flomoxef, SCE 2787, cefpirome, cefepime, latamoxef, cefotaxime and of piperacillin plus tazobactam were comparatively evaluated by their in vitro activity against 1119 clinical isolates of 83 bacterial species. Escherichia coli, Klebsiella spp. Enterobacter sakazakii, Proteus spp. and Shigella spp. were about equally susceptible to the cephalosporins (MIC90: 0.06 to 0.5 mg/l), while the MIC90 for piperacillin plus tazobactam was between 2 and 16 mg/l. Enterobacter cloacae, Enterobacter aerogenes and Serratia spp. were most susceptible to SCE 2787, cefpirome and cefepime (MIC90: 0.06 to 2 mg/l) followed by latamoxef, cefotaxime, flomoxef and piperacillin plus tazobactam. For Citrobacter spp., Providencia spp. and Yersinia enterocolitica MIC90 were between 0.06 and 0.5 mg/l. Flomoxef was between 2 to 4 log2 less active against these species but more active than piperacillin plus tazobactam (MIC90: 2 and 8 mg/l). Morganella morganii and Hafnia alvei were most susceptible to cefepime, cefpirome and latamoxef (MIC90: 0.13 to 0.5 mg/l) while cefotaxime (MIC90: 8 mg/l) and piperacillin plus tazobactam (MIC90: 8 and greater than 64 mg/l) were the least active compounds. SCE 2787, cefepime and cefpirome were the most potent beta-lactams against the majority of the 13 species of non-fermentative bacilli (NFB) investigated (MIC90: 0.5 to 16 mg/l). The oxacephems were the least active compounds against NFB. Cefepime was the most active of the compounds included against Pseudomonas aeruginosa (MIC90: 16 mg/l). Haemophilus spp., Neisseria gonorrhoeae and Bordetella pertussis were most susceptible to cefotaxime (MIC90: 0.03 to 0.06 mg/l). Latamoxef had the lowest activity of all compounds against gram-positive cocci. Flomoxef was the most active compound against penicillinase producing Staphylococcus aureus and about equally active as the other betalactams against methicillin susceptible staphylococci of other staphylococcal species.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Bacterial Agents↗

An IS1-like element is responsible for high-level synthesis of extended-spectrum beta-lactamase TEM-6 in Enterobacteriaceae.

Resistance of Escherichia coli strain HB251 to the newer beta-lactam antibiotics, in particular ceftazidime and aztreonam, results from production of the extended-spectrum beta-lactamase TEM-6. The corresponding structural gene, bla(T)-6, and its promoter region were amplified by the polymerase chain reaction. Analysis of the sequence of the amplification product showed that bla(T)-6 differed by two nucleotide substitutions from bla(T)-1, the gene encoding TEM-1 penicillinase in plasmid pBR322. The mutations led to the substitution of a lysine for a glutamic acid at position 102 and of a histidine for an arginine at position 162 of the unprocessed TEM-1 protein. The presence of a 116 bp DNA insert upstream from bla(T)-6 resulted in the creation of hybrid promoter P6 in which the -10 region was that of TEM-1 promoter P3 whereas the -35 canonical sequence TTGACA was provided by the right end of the insert. P6 was found to be 10 times more active than P3 and to confer higher levels of antibiotic resistance upon the host. Analysis of the sequence of the insert indicated that the 116 bp fragment is related to insertion sequence IS1 but differs from it by three internal deletions that removed regions encoding the transposase. The distribution of the IS1-like element in clinical isolates of Enterobacteriaceae was studied by the polymerase chain reaction and by DNA-DNA hybridization. The element appeared to be widespread and was detected in strains producing TEM-6 or other TEM variants.

Base Sequence↗

[The effect of sulbactam on the in vitro activity of mezlocillin, piperacillin and cefotaxime].

The in vitro activity of mezlocillin (MZL, CAS 51481-65-3), piperacillin (PIP, CAS 61477-96-1) and cefotaxim (CTX, CAS 63527-52-6) alone and in combination with sulbactam (SBT; CAS 68373-14-8) against mezlocillin-resistant pathogens was determined in a multicenter study. A total of 870 strains were investigated (481 Enterobacteriaceae, 57 Pseudomonas aeruginos, 41 Acinetobaster spp., 194 Bacteroides fragilis, and 97 Staphylococcus spp.). Determinations of MIC were performed according to DIN-guidelines (agar-dilution method for aerobes and microbroth-dilution method for anaerobes). Sulbactam was added in fixed concentrations of 5 mg/l and 10 mg/l. In all sulbactam-combinations examined mean MIC as well as MIC50 and MIC90 were reduced compared to the respective values for the antibiotics alone. Consequently, percentages of susceptible strains increased significantly: i.e. for Enterobacteriaceae: MZL 1% vs. MZL + 10 mg/l SBT 53%; PIP 4% vs. PIP + 10 mg/l SBT 54%; CTX 52% vs. CTX + 10 mg/l SBT 68%. The effect of sulbactam was most pronounced in Bacteroides spp. with an increase in susceptible strains from 2% to 97% for MZL, from 6% to 95% for PIP and from 7% to 98% for CTX. The results indicate that by adding sulbactam the in vitro activity of mezlocillin, piperacillin and cefotaxim against resistant pathogens is augmented significantly. In addition, the spectrum of antibacterial activity is extended to anaerobic pathogens such as Bacteroides spp. The availability of sulbactam as a monosubstance for combination with various beta-lactam-antibiotics thus represents a useful improvement of therapeutic options in bacterial infections.

Acinetobacter↗

[Effectiveness and tolerance of cefixime in bacterial infections in the ENT area].

Clinical efficacy and tolerance of cefixime were investigated in an open, uncontrolled trial. 200 mg of cefixime were applied twice daily, duration of therapy was between eight and 14 days (mean value 10.1 days, standard deviation +/- 1.4 days). Ten male patients (mean age 42.7 years) and 19 female patients (mean age 34.4 years) were enrolled. Cure or improvement was observed in all 27 patients evaluable for efficacy of treatment. Bacteriological results based on 15 bacteriologically evaluable patients were: elimination of the initial pathogen 60%, persistence 40%. Unwanted side effects and their incidence among the 29 patients evaluable for tolerance were: diarrhoea eight patients (mild to moderate, limited to three to four days on average), nausea and vomiting one patient, discharge and pruritus one patient.

Adult↗

[Antibacterial activity and beta-lactamase stability of eleven oral cephalosporins].

Oral cephalosporins (cefixime, cefdinir, cefetamet, ceftibuten, cefpodoxime, loracarbef, cefprozil, cefuroxime, cefaclor, cefadroxil and BAY 3522) were compared by their antibacterial profile including stability against new beta-lactamases. Both activity and antibacterial spectrum of compounds structurally related to third generation parenteral cephalosporins (of the oximino class) were superior to established compounds. Activity against staphylococci was found to be highest for cefdinir, cefprozil and BAY 3522. Cefetamet, ceftibuten and cefixime demonstrate no clinically meaningful antistaphylococcal activity while the other compounds investigated demonstrate intermediate activity. The antibacterial spectrum was broadest for cefdinir and cefpodoxime. New oral cephalosporins are equally inactive as established compounds against Enterobacter spp., Morganella, Listeria, Pseudomonas and Acinetobacter spp., methicillin-resistant staphylococci, Enterococcus spp., penicillin-resistant pneumococci and anaerobes. New extended broad-spectrum betalactamases (TEM-3, TEM-5, TEM-6, TEM-7, SHV-2, SHV-3, SHV-4, SHV-5, CMY-1, CMY-2, and CTX-M) are active against the majority of oral cephalosporins. Ceftibuten, cefetamet, cefixime and cefdinir were stable against some of these enzymes even to a higher extent than parenteral cephalosporins. New oral cephalosporins should improve the therapeutic perspectives of oral cephalosporins due to their higher activity against pathogens marginally susceptible to established compounds (higher multiplicity of maximum plasma concentrations over MICs of the pathogens) and furthermore by including in their spectrum organisms resistant to established absorbable cephalosporins (e.g. Proteus spp., Providencia spp., Citrobacter spp., and Serratia spp.).

Administration, Oral↗

Novel resistance to imipenem associated with an altered PBP-4 in a Pseudomonas aeruginosa clinical isolate.

A Pseudomonas aeruginosa (isolate 416) from a patient with pneumonia, was initially susceptible to imipenem (MIC: 2 mg/l) but became resistant to this antibiotic (isolate 470, MIC: 32 mg/l) during imipenem therapy. Treatment failed. No parallel increases in MIC were observed for other antimicrobials tested. Isolates 416 and 470 shared the same pyocin type and serotype, produced small amounts of an inducible beta-lactamase, and had similar lipopolysaccharide compositions. On electrophoresis of outer membrane proteins, the porin F, identified by the monoclonal antibody MA4-4, was expressed similarly by the two isolates but the production of one band (apparent molecular weight: 47,000) was diminished in isolate 470. [14C]-Imipenem labelling of intact cells proceeded more slowly in 470 than in 416, especially when bacterial cells were treated by antibody MA4-4 to block the porin F channel. [14C]-Imipenem labelling of penicillin binding proteins (PBP) showed that the band identified as PBP-4 bound markedly less radioactivity in isolate 470 than in 416. After isolate 470 was passaged several times in antibiotic-free broth, the imipenem MIC was decreased from 32 to 8 mg/l, and the [14C]-imipenem PBP pattern recovered the initial profile as exhibited by isolate 416. Two resistance mechanisms, affecting imipenem electively, could have combined their effect in the post-therapy isolate, altered target protein and reduced permeability.

Animals↗

[Intragastric formation of ammonia in Campylobacter pylori associated gastritis. Diagnostic and pathogenetic significance].

The diagnostic relevance of measurement of ammonia (NH3) in not stimulated gastric juice in patients with campylobacter pylori associated gastritis (CPAG) is in discussion. The role of CP-urease induced NH3 in pathogenesis of active gastritis is unclear. In answering to this questions we evaluated the sensitivity and specifity of NH3-test and CLO-test in cases of CPAG (n = 50), non CPAG (n = 16) and normal gastric mucosa (n = 20). We found a 88% sensitivity and a 86% specifity for NH3-test, a sensitivity for CLO-test of 80% and a specifity rate of 87%. NH3-test correlated well with CLO-test (n = 51, p less than 0.01) and semiquantitative histological identification of CP (p less than 0.01, n = 22). On the other hand we tried to correlate the amount of NH3 in the gastric juice and the histological degree of gastritis activity (infiltration of leucocytes of the lamia propria) in CPAG (n = 78) and Non-CPAG (n = 32) and before and after therapy in CPAG (n = 9) with bismuthsubnitrate (2 g/d, 14 d). There was no correlation between the amount of NH3 and the degree of active chronic gastritis in patients with CPAG (with or without therapy) and patients with non CPAG. It seems that NH3 has a diagnostic but no pathogenetic role in the process of inflammatory activity of CPAG.

Ammonia↗

[In-vitro activity of enoxacin: a multicenter study].

The in vitro activity of enoxacin was tested in 14 German microbiological centers shortly after the introduction of the drug in Germany. 2748 unselected clinical isolates including 15 bacterial species were analysed using microtiter plates. The MIC90-values were as follows: Staphylococcus aureus 4 mg/l, Enterococcus faecalis 16 mg/l, Enterobacteriaceae 0.5 mg/l, Pseudomonas aeruginosa 8 mg/l. There is good correlation between these results and those of former investigations. It is known that quinolones are only moderately active against enterococci. 8.5% of S. aureus, and 1.4% of Enterobacteriaceae were found to be resistant (MIC greater than 4 mg/l). As to P. aeruginosa, the study revealed that despite a generally low rate of resistance in specific clinical settings, specific problems can arise: in one institution, the MIC90 of P. aeruginosa was 32 mg/l, with a resistance rate of 56.1% (n = 57). In the other centers the MIC90 was 2 mg/l and the resistance rate 5.0% (n = 302). In the first center, many of the isolates were from paraplegic patients or patients with cystic fibrosis pretreated with quinolones. This study will be repeated in two years' time in order to determine an eventual change in resistance.

Bacteria↗

In-vitro activity of meropenem imipenem, the penem HRE 664 and ceftazidine against clinical isolates from West Germany.

The antibacterial activity in vitro of meropenem was compared with another carbapenem, imipenem, the penem HRE 664, and ceftazidime. MICs were not influenced by pH nor by inoculum size below 5 X 10(5) cfu/ml: higher inocula caused a modest increase in MIC. Cation supplementation of Mueller-Hinton broth was without effect. Meropenem was more active than imipenem and the other comparative agents against the majority of Gram-negative species (in particular proteus, providencia, morganella, haemophilus, neisseria and Pseudomonas aeruginosa, including isolates from patients with cystic fibrosis). Against Gram-positive organisms, the activity of meropenem was equal to or slightly less that of imipenem. Neither meropenem nor imipenem were influenced by the extended spectrum beta-lactamases that confer resistance to third generation cephalosporins produced by Escherichia coli, Klebsiella pneumoniae, K. oxytoca or Serratia marcescens.

Anti-Bacterial Agents↗

[A rapid urease test in Campylobacter pylori colonization of the gastric mucosa].

Biopsies from the gastric mucosa (antrum, corpus) of 145 patients investigated by endoscopy were analysed for Campylobacter pylori. The results of bacteriological, histological, enzymatic and chemical methods were compared. Urease activity was determined both in biopsies (CLO-test) and in gastric secretion. Furthermore, the concentration of urea was measured in gastric secretion. 71% of gastritis, 86% of ulcus duodeni and 83% of ulcus ventriculi diagnosed by endoscopy produced positive histological and/or cultural results, while 100% of control persons exhibited negative for both parameters. The sensitivity of the CLO-test (n = 112) was 95% and its specificity 78% when compared with bacteriological and histological results. The majority of false positive results was due to delayed and incomplete reactions. However, when compared with endoscopic-histological results the specificity of the CLO-test was 100%. The results of a modification of CLO-test (without culture medium) were up to 5 hours comparable. There was no positive correlation between the concentration of urea in gastric secretion and the histological or cultural identification of Campylobacter pylori. However, the measurement of ammonia turned out to be promising (sensitivity 80%). None of the tests was sufficiently specific on its own, whereas a 100% specificity was achieved when both the CLO-test and the determination of ammonia in gastric secretion were performed.

Adult↗