CP-45,899 {3,3-dimethyl-7-oxo-4-thia-1-azabicyclo(3.2.0)heptane-2-carboxylic acid, 4,4-dioxide, [2S-(2a,5a)]} is an irreversible inhibitor of several bacterial penicillinases and cephalosporinases. In the presence of low concentrations of CP-45,899, ampicillin and other f,-lactams readily inhibit the growth of a variety of resistant bacteria that contain ,-lactamases. 899 In vitro susceptibility studies were performed in brain heart infusion broth as the basal medium. The broth was enriched with 5% (vol/vol) sheep blood for studies with Streptococcus pyogenes and 5% Fildes plus 2% IsoVitaleX for Haemophilus influenzae. Tests with Neisseria gonorrhoeae were performed on gonococcus agar base (BBL) supplemented with hemoglobin and IsoVitaleX. Studies with Bacteroides fragilis were carried out in prereduced brain heart infusion as described in the Anaerobe Laboratory Manual (3); incubation was in an 80% N2-10% C02-10% H2 gas mixture either in an anaerobic chamber or in GasPak jars equipped with gas-exchange capability.Methods. Minimal inhibitory concentrations (MICs) of antibiotics in combination with CP-45,899 were determined using a 7-by-7-concentration grid protocol in broth culture, as described by Sabath (8), with an inoculum of-i0 colony-forming units per ml.Testing for synergy against B. fragilis was performed by an agar dilution method similar to the broth dilution method.p8-Lactamase studies. The hydrolysis of ampicillin and penicillin G was determined by the microiodometric method of Novick (5). Cephaloridine hydrolysis was measured by following the decrease in ultraviolet absorbance at 255 nm (6). Conditions for both assays were identical: 0.5 M potassium phosphate, pH 6.5, and 37°C. Reactions were initiated by the addition of the cell-free ,B-lactamase, except in the case of preincubation experiments in which the inhibitor and enzyme were incubated together in the assay mixture for 10 min before initiation of the reaction by addition of substrate. With the cell-free extracts of Staphylococcus aureus, Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa, the substrate was

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OBJECTIVES-Acute compartment syndrome (ACS) is the result of decreased perfusion pressure (PP) and the diagnosis frequently requires invasive monitoring. Our objective was to test a new noninvasive ultrasound device for correlating PP with measurements of fascial displacement in a controlled porcine model of ACS. We hypothesized that fascial displacement in experimental compartments with impaired PP would be significantly greater than that in control compartments with normal baseline PP.METHODS-ACS was generated in right anterior compartments of seven anesthetized pigs while contralateral compartments served as normal controls. Intramuscular pressure (IMP) in all compartments was monitored by slit catheters while IMP in experimental compartments was elevated in 10 mmHg increments by infusing 0.045% albumin in saline. A non-invasive ultrasound device continuously recorded fascial displacement corresponding to arterial pressure pulses in all compartments. Mean fascial displacement amplitude was grouped by PP and analyzed using twoway repeated measures ANOVA and contrast analysis.RESULTS-As PP ranged from 80 to -40 mmHg, the change in fascial displacement of the infused compartments was significantly greater than that in the control compartments (ANOVA, p = 0.03). At each PP increment between 40 and -20 mmHg, fascial displacement in the infused compartments was significantly greater than that in the control compartments (contrast analysis, p < 0.014).CONCLUSIONS-Fascial displacement is significantly greater in muscle compartments with decreased PP. Furthermore, changes in PP are associated with changes in fascial displacement over a clinically relevant range of PP, making this non-invasive technique potentially useful for monitoring in ACS.

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Subtherapeutic levels of oxytetracycline in animal feeds have been evaluated to determine their influence on the relative quantity, prevalence, shedding, and antibiotic susceptibility of Salmonella typhimurium in swine, calves, and chickens, when compared with nonmedicated controls. The medicated groups were fed rations containing oxytetracycline commencing 5 days prior to oral inoculation with S. typhimurium and continuing through a 28-day post-inoculation period. Colonization ofS. typhimurium occurred in all three animal species as evidenced by clinical signs ofinfection and/or colony counts in feces measured on seven separate occasions over the 28-day observation period. The accumulated data demonstrate that the subtherapeutic use of oxytetracycline did not bring about any increases in the quantity, prevalence, or shedding of S. typhimurium in swine, calves, and chickens. In fact, the medication generally brought about a decrease in the percentage of animals carrying S. typhimurium during the study period. In contrast to results in swine and calves, there was a significant occurrence of S. typhimurium resistance to oxytetracycline in chickens. Resistant colonies were isolated from chickens sporadically but never on more than two consecutive test periods. These isolates were also resistant to streptomycin, but not to the other six antibiotics tested. The population of resistant S. typhimurium isolated from medicated chickens was no larger than that of susceptible S. typhimurium isolated from the nonmedicated animals. It is concluded that no evidence has been obtained which would relate the continuous low-level feeding of oxytetracycline for a 4-week period to an increased incidence of disease in animals or as a hazard to humans.