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In vitro and in vivo activities of amikacin and imipenem alone, and in combination, were studied against an extended-spectrum beta-lactamase-producing Klebsiella pneumoniae strain. The strain was in vitro susceptible to both antimicrobials at 10(5) and 10(7) CFU/mL. In time-kill studies amikacin, imipenem, and amikacin plus imipenem decreased the bacterial counts; difference between the bactericidal effects was not observed. Chequerboard technique showed no interaction between the tested drugs. Mice infected with 10(7) CFU/g of the K. pneumoniae were treated by amikacin (15 mg/kg every 8 h), imipenem (40 mg/kg every 4 h), or amikacin plus imipenem for 24 h. Blood bacterial counts in the group treated with amikacin plus imipenem did not differ significantly from the groups treated with amikacin or imipenem alone. Combination of amikacin and imipenem did not demonstrate any advantage over imipenem alone either in vitro or in vivo.

The simulation of human serum levels is essential in animal models to extrapolate the experimental results to clinical practice. Administration of a nephrotoxic drug such as cisplatin can be used to cause renal dysfunction as an approach to mimic human serum levels of renally excreted drugs. We aimed to determine the dose of cisplatin that did not affect the survival rate of mice and to achieve human-like serum concentrations of cefepime. Different doses of cisplatin (0, 10, 14, 18, 22 and 26 mg/kg) were given by intraperitoneal (i.p.) injection to mice three days prior to the i.p. administration of 80 mg/kg cefepime. With cisplatin doses of 18 and 22 mg/kg, the half-life of cefepime was significantly prolonged ( P

Activities of ciprofloxacin and levofloxacin against an SHV-5 extended-spectrum s-lactamase (ESBL)-producing Klebsiella pneumoniae strain were studied in vitro and in vivo in septic mice using a high inoculum. Susceptibility to ciprofloxacin and levofloxacin was independent of the inoculum size. In killing curve studies, after 24 hours the initial 7.69 log 10 CFU / ml increased in the control to 9.34, while it was reduced to 4.83 by ciprofloxacin and to 4.25 by levofloxacin. Mice were infected with 10 7 CFU / g of K. pneumoniae intraperitoneally. Treatment started 2 hours later, when the mean blood bacterial counts were 7.33 log 10 CFU / ml, and lasted for 26 hours from the time of infection. Blood bacterial count was reduced from 7.33 log 10 CFU / ml to 4.08 log 10 CFU / ml by ciprofloxacin (20mg / kg / 6 hours), and to 3.60 log 10 CFU / ml by levofloxacin (50 mg / kg / 6 hours) 8 hours after the infection, which differed significantly from the infected untreated group. Ciprofloxacin and levofloxacin prolonged significantly the survival of mice compared with the infected untreated group (p < 0.001 for both groups). There were not significant differences either in the survival (p=1.0) or in the blood bacterial counts (p=0.216 after 8 hours) between ciprofloxacin and levofloxacin group. Based on these results both ciprofloxacin and levofloxacin could be alternative therapeutic agents for the infection caused by ESBL-producing Klebsiella strains.

The in vitro and in vivo effectiveness of amikacin, cefepime, and imipenem was studied using a high inoculum of an extended-spectrum β-lactamase-producing Klebsiella pneumoniae strain. An in vitro susceptibility test at the standard inoculum predicted the in vivo outcome of amikacin or imipenem while it did not do so for cefepime due to the inoculum effect.

Following intraperitoneally (i.p.) applied treatment with 12.5 mg/mouse prednisolonum (PRD) no bacterial translocation (BT) was observed in mice. The PRD treatment applied in combination with lymphotropic cytostatics as dianhydrogalactitol (30 mg/kg i.p.) or chlorpromazine (75 mg/kg i.p.) both causing BT, did not increase the mice's drug sensitivity to the used agents. According to our results, PRD can be suitable for combined application with other immunosuppressive agents as it can increase immunosuppression without increase of side-effects such as those induced by bacterial translocation.

Comme consequence de l'interaction de la maladie homologue produite dans des souris F1 hybrides adultes et de l'infection avec le virus de la choriomeningite lymphocytique, les signes histologiques de la maladie homologue etaient aggraves. D'autre part, une action protectrice inversement proportionnelle a la gravite des alterations histologiques attribuables a la maladie homologue vis-a-vis des manifestations neurologiques de l'infection avec ce virus etait evidente.

In neonatal thymektomierten Mausen wurden nach 6–7 Wochen rontgenologisch sowie histologisch das «wasting syndrome» und schwere Knochenatrophien beobachtet. Der Mechanismus der beobachteten enchondralen Ossifikationsstorung wurde diskutiert.

Nachweis, dass Mause nach i.v. oder i.p. Injektion homologer Milzzellen eine Lymphopenie, verbunden mit Gewichtsverlust, entwickeln. Diese Tiere reagieren nachher auf einen Stress in Form von Abkuhlung oder Schutteln nicht mehr mit einem weiteren Lymphozytenabfall.

Chez des souris hybrides F1 adultes, subissant la maladie homologue produite par l'injection de cellules parentales, la mortalite precoce et les manifestations neurologiques d'une infection due au virus de la choriomeningite lymphocytique etaient reduits. D'autre part, le developpement des symptomes caracteristiques du «runting» apparait comme accelere et aggrave par l'infection produit par ce virus.

Es wurde eine Praponderanz der neutralen Mukopolysaccharide in der Epiphysealplatte der neonatal thymektomierten Mause beobachtet und das Phanomen diskutiert.

Immunpathologische Untersuchungen an Mausen, welchen i.p. Milzzellen von Spendertieren injiziert wurden. Rontgenologisch und histomorphologisch wurden Knochenatrophien festgestellt und es kam zu verzogerter Ossifikation sowie zu einer allgemeinen Wachstumsverzogerung.

Es wurde festgestellt, dass die Virusinfektion in mit LCM-Virus intrazerebral infizierten Mausen bei Phytohamagglutinin-Behandlung gleich verlauft wie in unbehandelten Kontrolltieren. Dies stutzt die Annahme, Phytohamagglutinisierung vermindere die immunologische Reaktivitat des Organismus nicht.