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Biomedical subjects

J W Sensakovic

Publications and source records attributed to J W Sensakovic.

10 recordsLinked to original sources

Oral antibiotic treatment of infectious diseases.

The use of antimicrobial agents (i.e., penicillins, cephalosporins, macrolides, aminoglycosides, tetracyclines, quinolones) have continued to grow at an astounding rate. Centers for Disease Control and Prevention estimates are of some 150 million prescriptions annually in the United States, amounting to some 50 millions pounds of antibiotics annually being used in the United States with some 15 to 17 million pounds being used in livestock and agriculture alone. These large numbers serve as indicators for caution and concern. Most oral antibiotics are prescribed for respiratory tract infections, more than half of which are probably viral, for which antimicrobials are not necessary. This overprescribing is noted at a time when increasing antimicrobial resistance is being recognized in hospital settings as well as in the community. The dilemma for the practitioner is to be able to use antibiotics efficaciously and prevent overusage and overprescribing.

Administration, Oral↗

Beta-lactamase inhibitor combinations.

The beta-lactamase inhibitor combinations present a novel approach to the problem of beta-lactamase-induced resistance to antibiotics. These agents are derived from the generally safe beta-lactam class of antibiotics. They are all principally excreted through the kidneys and require dosage adjustment in the face of significant renal insufficiency. They show significantly increased activity against methicillin-sensitive S. aureus, H. influenzae, B. catarrhalis, and B. fragilis. The activity against Enterococcus, Pseudomonas, and most gram-negative bacilli, however, remains limited to that of the respective antibiotic component. Although shown to be clinically useful in a variety of clinical situations, they appear to be most useful for skin and soft tissue infections and lower respiratory tract infections as well as intra-abdominal and gynecologic infections caused by susceptible pathogens.

Anti-Bacterial Agents↗

Pentamidine treatment of Pneumocystis carinii pneumonia in the acquired immunodeficiency syndrome. Association with acute renal failure and myoglobinuria.

A 31-year-old man with acquired immunodeficiency syndrome and biopsy-proved Pneumocystis carinii pneumonia developed acute renal failure, elevated creatinine kinase levels, and myoglobin in both serum and urine while being treated with pentamidine. The patient was receiving no other nephrotoxic medications at the time, and these unusual complications were directly related to the pentamidine.

Acquired Immunodeficiency Syndrome↗

In vivo distribution of Pseudomonas aeruginosa slime glycolipoprotein: association with leukocytes.

Intraperitoneal injection of slime glycolipoprotein (GLP) from Pseudomonas aeruginosa induced leukopenia and death of mice, similar to the effect of infection with viable organisms. Differential counts established that the leukopenia was characterized by a decrease in the number of polymorphonuclear leukocytes, followed by death of mice. Mice immunized with GLP survived challenge and responded with a leukocytosis that had a substantial increase in circulating polymorphonuclear leukocytes. Leukocytes from GLP-injected mice were agglutinated by anti-GLP serum, indicating an association between GLP and leukocytes. Other results indicated that 14C-labeled GLP is deposited mainly in the liver. Normal leukocytes labeled with 51Cr were injected intravenously into mice receiving an intraperitoneal injection of GLP. As with GLP, the 51Gr-labeled leukocytes were sequestered in the liver. These results indicate that GLP enters the blood stream and becomes associated mainly with neutrophils, and that the neutrophil-GLP complex is deposited in the liver, possibly accounting for the leukopenia in mice.

Agglutination Tests↗

Glycolipoprotein from Pseudomonas aeruginosa as a protective antigen against P. aeruginosa infection in mice.

After primary subcutaneous immunization of rabbits with glycolipoprotein from Pseudomonas aeruginosa BI, indirect hemagglutinating and bacterial agglutinating activities appeared in the antiserum 6 days after immunization and reached a peak between 15 and 20 days. Both these in vitro activities paralleled in vivo antipseudomonas-induced leukopenia and mouse passive-protection activities. Further experiments indicated that a functional association exists between the hemagglutinating and passive-protection activities, and that passive protection depends on activity levels in the plasma rather than in the peritoneum. After intraperitoneal injection in mice, in vitro and in vivo activities of antiglycolipoprotein serum declined in the peritoneal cavity as the plasma levels increased. After intravenous injection of the antiglycolipoprotein serum, initially high levels of in vitro and in vivo activity declined at approximately equal rates. Immunoglobulin G (IgG) and immunoglobulin M (IgM) fractions from 15-day antiglycolipoprotein serum were assayed for biological activity. Most of the hemagglutinating and bacterial agglutinating activity and all of the mouse passive-protection activity were found in the IgM fraction. Assay of antiglycolipoprotein serum after 2-mercaptoethanol inactivation of IgM showed that most of the in vitro and all of the passive-protection activities had been destroyed, again locating these activities principally in the IgM fraction of the original antiserum.

Agglutinins↗

Biological activity of fragments derived from the extracellular slime glycolipoprotein of Pseudomonas aeruginosa.

Glycolipoprotein, obtained from the extracellular slime layer of Pseudomonas aeruginosa, was purfied and subjected to chemical and enzymatic treatment in an attempt to assign certain of its biological activities to chemical moieties comprising the glycolipoprotein molecule. Treatment of the glycolipoprotein with phenol, although removing all detectable protein, yielded a fragment capable to exerting the biological activities associated with the untreated glycolipoprotein (leucopenia, lethality, inhibition of phagocytosis, antigenic specificity). Acetic acid treatment resulted in a fragment composed mainly of carbohydrate and a small amount of protein, but no detectable lipid. This fragment was devoid of leucopenic and lethal activity, but retained antigenic specificity and the ability to inhibit phagocytosis. The fragments release from the glycolipoprotein after treatment with phage 2-depolymerase were low-molecular-weight products and were devoid of the biological activities associate with the glycolipoprotein.

Animals↗

Slime of Pseudomonas aeruginosa: in vivo production.

Indirect hemagglutination inhibition tests were employed to detect slime in concentrations as low as 1 mug/ml. Increasing concentrations of slime resulted in proportionately greater inhibition of hemagglutination. Peritoneal aspirates and plasma of mice injected with slime were shown to exhibit the inhibitory activity of slime. The rapid dissemination of slime into the peripheral circulation was also indicated by the hemagglutination of mouse erythrocytes by specific anti-slime serum. By similar methods, the inhibitory activity of slime was also detected in peritoneal aspirates and plasma of mice infected with lethal doses of viable Pseudomonas aeruginosa. Furthermore, the inhibitory activity was found to increase with time after viable cell infection, whereas such increases were not detected after the injection of heat-killed organisms. Ferritin-labeled slime antibodies were found to completely surround cells of Pseudomonas aeruginosa obtained from the peritoneal cavity of mice 5 h postinfection.

Animals↗