[Susceptibility to selected coagulase-negative chemotherapeutic agents of methicillin resistant staphylococci isolated from clinical materials in 1997-1998]. / Wrazliwosc na wybrane chemioterapeutyki koagulazo--ujemnych gronkowców opornych na metycyline izolowanych z materialu klinicznego w latach 1997-1998.

The study was aimed at assessment of the sensitivity of methicillin-resistant coagulase-negative staphylococci isolated from clinical material in 1997/1998 to selected chemotherapeutic agents. The investigated material comprised 96 methicillin-resistant coagulase-negative staphylococci from hospital and ambulatory infections isolated during the period from April 1997 to May 1998. Species affiliation was determined by classical identification methods and commercial diagnostic tests for identification of staphylococci. Methicillin resistance was determined by agar disk-diffusion method and screening. Sensitivity to chemotherapeutics was determined by agar disk-diffusion method and agar dilution methods. All the investigated strains were sensitive to nitrofurantoin, furazolidone and vancomycin. To teicoplanin--the second glycopeptide antibiotic--84% strains were sensitive, whereas the percentages of resistant and moderately sensitive strains amounted to 5.2% and 10.4%, respectively. 85% and 82% of coagulase-negative staphylococcal strains were sensitive to fusidic acid and mupirocin. Considerable differences were noted with respect to sensitivity to aminoglycoside group antibiotics. About 35% of strains were sensitive to gentamicin, and 90% sensitive to netilmicin. Ca. 40% of coagulase-negative staphylococci were resistant both to cotrimoxazole and trimethoprim, which, in view of 98% resistance to the second component of cotrimoxazole, may be associated with the activity of only one of the components of the drug--trimethoprim.

[Susceptibility to selected chemotherapeutics of Staphylococcus aureus strains resistant to methycyline isolated from clinical materials in the years 1991-1992 and 1997]. / Wrazliwosc na wybrane chemioterapeutyki szczepów Staphylococcus aureus opornych na metycyline izolowanych z materialu klinicznego w latach 1991-1992 i w roku 1997.

The susceptibility to selected chemotherapeutic agents was determined in 100 strains of Staphylococcus aureus methicillin-resistant (MRSA) isolated from clinical materials in 1991-1992 (50 strains) and in 1997 (50 strains). Two methods were used for the determination: disc method and antibiotic dilution in agar. The minimal inhibitory concentration (MIC) was determined for vancomycin, teicoplanin, furazolidone, nitrofurantoin, ofloxacin, gentamicin, netilmicin and trimethoprim. The concentrations of the chemotherapeutics in the substrate ranged from 0.125 to 512 mg/l. The obtained results served for drawing of the following conclusions: all studied MRSA strains isolated in 1991-1992 and in 1997 were sensitive to glycopeptide antibiotics: vancomycin and teicoplanin, to nitrofurans: nitrofurantoin and furazolidone, and to fusidic acid. MRSA strains isolated in 1991-1992 were sensitive to ofloxacin, but in 1997 about 80% of the strains were resistant to that antibiotic, and this resistance was noted in S. aureus strains with homogeneous resistance to methicillin. Increasing frequency of resistance to mupirocin was found, in 1991-1992 4% of the strains were resistant, and in 1997 the resistance of MRSA to that antibiotic was found in 12%. No changes occurred in the sensitivity of staphylococci to trimethoprim/sulfamethoxazole (cotrimoxazole). About 94% of strains in 1991-1992 and 1997 were sensitive to that drug. The sensitivity to cotrimoxazole is connected with one of its components (trimethoprim), with 94% of MRSA strains sensitive to it.

[Microbial analysis of clinical material taken from patients at the Oncology Center, Maria Sklodowkda-Curie Institute in Warsaw in 1997]. / Mikrobiologiczna analiza materialu klinicznego pobranego od pacjentów Centrum Onkologii--Instytutu im. Marii Sklodowskiej-Curie w Warszawie w 1997 roku.

An analysis was carried out of the microbiological investigations of clinical material samples obtained from the patients of two oncology centres belonging to the Warsaw Oncology Centre. Microorganisms cultured from urine, blood, catheters, smears of wounds and other materials were analysed. From 4839 clinical material samples from the Ursynów centre 1755 bacterial strains were isolated. From 423 samples from the centre in Wawelska Street 171 strains were obtained. In infections of patients from the centres the number of Gram-positive cocci was twice that of Gram-negative rods. In the investigated clinical material S. aureus was the most frequently isolated Gram-positive coccus, while E. coli was the most frequent species among Gram-negative bacteria. In the infections of oncological patients a considerable frequency was noted of yeast-like fungi, especially C. albicans. Particularly disquieting was the increasing number of isolates of C. glabrata and C. krusei strains resistant to fluconazole.

[Does the appearance of pro-arrhythmic response to anti-arrhythmic drugs have prognostic significance?]. / Czy wystapienie reakcji proarytmicznej na lek przeciwarytmiczny ma znaczenie prognostyczne?

Study was undertaken to assess whether proarrhythmic response to antiarrhythmic drug is a risk factor for cardiac death in patients (pts) with ischaemic heart disease (IHD). In 782 pts with IHD and frequent and/or complex ventricular ectopic beats (VEB) 1041 drug tests guided by 24 hour Holter monitoring were conducted. The following drugs were assessed: propranolol, disopyramide, mexiletine, amiodarone. Pro-arrhythmia was defined according to Velebit: 1/greater than or equal to 4-fold increase in VEBs, 2/greater than or equal to 10-fold increase in repetitive forms of 3/new occurrence of ventricular tachycardia or ventricular fibrillation (VT/VF). Proarrhythmic effect was observed in 8.4% of pts and in 7.9% of drug tests. The frequency with individual drugs ranged from 5.7% to 9%. No drug was completely free of this type of reaction. Antiarrhythmic drugs inducing arrhythmogenic response were eliminated. Pts were followed-up for a mean of 22 months (range 1-49). Chronic antiarrhythmic treatment was conducted. Pts were discharged taking the agent deemed most effective for suppression of arrhythmia. Follow-up visits were made every 6-12 months. All cases of death were verified. In long-term observation cardiac death and sudden death occurred in 53 and 32 pts. With actuarial analysis (Kaplan-Meler method, log rank test) there was significant difference in cardiac death (p less than 0.05) of pro-arrhythmia (+) compared with ++pro-arrhythmia (-) pts at yr (11% v 4%, 7% v 3%) and 3 yr (24% x 11%, 16% v 7%). The relative importance of baseline clinical variables in predicting survival was assessed with a stepwise Cox regression.(ABSTRACT TRUNCATED AT 250 WORDS)

[Effect of beta adrenergic blocking drugs on the prognostic value of ST-segment depression during exercise electrocardiogram testing]. / Wplyw leków beta adrenolitycznych na wartosc prognostyczna obnizonego odcinka ST w elektrokardiogramie wysilkowym.

Exercise testing has been shown to be predictive for future cardiac events in patients with established diagnosis of coronary heart disease. Exercise test parameters associated with poor prognosis may be unreliable if patient is receiving beta adrenergic agents. The purpose of this study was: 1) to compare the results of exercise testing performed before and during beta blocking therapy, and 2) to determine the role of beta blockers in the prognostic significance of the ST-segment response recorded during exercise testing. The study population consisted of 518 patients (mean age 52 +/- 7 years) with coronary heart disease. The diagnosis was based on the presence of one of the following three criteria: 1) typical history and significant ST-segment depression on resting or exercise electrocardiogram, 2) history of myocardial infarction, 3) significant coronary angiographic abnormalities. In all patients symptom-limited exercise test was performed before and two weeks after the onset of beta blocker therapy. The data from the first and second tests were estimated for significance of differences between the mean values with following results: maximal heart rate--135 +/- 21 and 123 +/- 19 bpm (p less than 0.001), maximal work load achieved--98 +/- 43 and 109 +/- 44 W (p less than 0.001), maximal systolic blood pressure--171 +/- 28 and 163 +/- 26 mmHg (p less than 0.001). Occurrence of characteristic ST-segment depression was more frequent during the first than during the second test (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Proarrhythmic response to antiarrhythmic drug as a risk factor for sudden cardiac death in patients with ischemic heart disease.

The prognostic significance of arrhythmogenic response to an antiarrhythmic drug was studied. In 782 patients with ischemic heart disease (IHD) and frequent and/or complex ventricular premature beats (VPBs), 1,041 drug tests guided by 24-hour Holter monitoring were conducted. The following drugs were assessed: beta blockers, disopyramide, mexiletine, amiodarone. Proarrhythmia was defined as: (1) greater than 4-fold increase in VPBs, (2) greater than 10-fold increase in repetitive forms, or (3) new occurrence of ventricular tachycardia or ventricular fibrillation (VT/VF). During a follow-up of 1-49 months (mean 22) patients were treated with antiarrhythmic drugs found to be safe in control Holter monitoring. Proarrhythmic effects were observed in 8.4% of patients. No drug was completely free of this type of reaction. In long-term observation, cardiac death and sudden death occurred in 53 and 32 patients, respectively. With actuarial analysis (Kaplan-Meier method, log-rank test) there was a significant difference in cardiac death (P less than 0.01) and sudden death rate (P less than 0.05) of proarrhythmia (+) compared with proarrhythmia (-) patients at 1 year (11% vs 4%, 7% vs 3%) and 3 years (24% vs 11%, 16% vs 7%). Proarrhythmic response was an independent risk factor apart from myocardial infarction, VT/VF, ejection fraction less than 40% and QTc greater than 440 msec. Arrhythmogenic response to antiarrhythmic drugs seems to be an additional predictor of sudden death in IHD.

[Late ventricular potentials and ventricular arrhythmia in patients with stable ischemic heart disease]. / Pózne potencjaly komorowe i arytmie komorowe u pacjentów ze stabilna choroba niedokrwienna serca.

Ischaemic heart disease especially after previous myocardial infarction can predispose to the life-threatening ventricular arrhythmias. Late potentials (LP) are confirmed parameters predicting patients prone to sudden cardiac death in ventricular arrhythmias mechanism. Late potentials registered noninvasively from the body surface were analysed in 86 patients with stable ischaemic heart disease (67 males and 19 females aged 35-67, mean 53 years). Registration of signal average electrocardiograms (SA-ECG) were performed by Simson technic (X, Y, Z orthogonal leads) using identical analysing systems and quantitative SA-ECG criteria in all three participating centers. In all patients ventricular arrhythmias detected on 24-hour ecg Holter monitoring were assessed. The localisation of previous myocardial infarction and echocardiographic assessment of left ventricular function were also analysed in each case. The results of SA-ECG were correlated with these clinical findings. Late potentials were detected (according to two or three accepted criteria) in 16 pts (19%), in 53 pts (61%) SA-ECG were normal but in other 17 pts (20%) abnormal SA-ECG (according to only one criterium) were registered. Out of these 17 pts with abnormal SA-ECG, 14 pts had prolonged filtered QRS duration as the only incorrect SA-ECG parameter. Comparative analysis between studied groups shows higher incidence of previous Q-wave myocardial infarctions in patients with LP and with abnormal SA-ECG than in patients with normal SA-ECG (63% and 71% vs 43% respectively; p less than 0.01). Ventricular arrhythmias observed in studied patients occurred with similar frequency in all groups however in patients with LP and with abnormal SA-ECG complex ventricular arrhythmias were more common than in group with normal SA-ECG (56% and 53% vs 49% respectively: NS).(ABSTRACT TRUNCATED AT 250 WORDS)

[Cordipine in the treatment of patients with exacerbated coronary disease]. / Cordipina w leczeniu chorych z choroba wiencowaw fazie zaostrzenia.

The results of pharmacological treatment are presented in a group of 60 patients with exacerbation of coronary disease. The patients were divided into two subgroups: subgroup 1 of 26 patients with intensification of angina of effort, subgroup II of 34 patients with unstable angina. Combined pharmacological treatment was given: nitrates, B-adrenolytic drugs and nifedipine (Cordipin, Krka) Addition of Cordipin produced clinical and electrocardiographic improvement in 44 cases (73%): all patients in subgroup I and 18 (53%) in subgroup II. Cordipin was well tolerated, and produced no serious side effects.

The ultrastructure of Penicillium chrysogenum in the course of benzyl-penicillin biosynthesis.

The find structures of high- and low-yield mutants of Penicillium chrysogenum, producing 100 and 10,000 units/ml of penicillin G, were compared. The cells of both mutants demonstrated a typical eukaryotic ultrastructure. In the cytoplasm nuclei, mitochondira, lipid bodies, endoplasmic reticulum, and Golgi vesicles were observed. In the cells of high-yield mutant, during the biosynthesis of penicillin, the number of lipid bodies decreased. It is possible that the lipids are metabolized in the process of biosynthesis of penicillin. In the cytoplasm more multivesicular bodies and small vesicles, about 40 nm in diameter, could be seen. These Golgi vesicles, present in largest number in cells of high-yield mutant, fuse with the cell membrane and play an important role in the transport of penicillin from the cytoplasm to the cell environment. The cell walls of the high-yield mutant become three times thicker during the antibiotic biosynthesis. No comparable changes were observed in the ultrastructure of the low-yield mutant. The cell wall thickness did not increase, the cytoplasm contained few Golgi vesicles only, and the lipid bodies can be seen in all cells.

The site of benzyl penicillin accumulation in Penicillium chrysogenum.

Benzyl penicillin was localized in cells of Penicillium chrysogenum by means of enzymatical and immunological methods, enabling the determination of minute amounts of penicillin. The reactions were performed on ultrathin sections. They allow to determine the antibiotic inside of the cells. The results indicate that benzyl penicillin is present in the vesicles belonging to the Golgi apparatus. Benzyl penicillin is transported from the cytoplasm outside the cell membrane by the Golgi vesicles.