Antibiotic review performed by a pharmacy and therapeutics subcommittee.
Explore the source record for details and available documents.
Anti-Bacterial Agents↗
Biomedical subjects
R Ramphal
Publications and source records attributed to R Ramphal.
Comparative efficacy of piperacillin and penicillin G in treatment of gonococcal urethritis.
The comparative efficacy of 2 g of piperacillin and 4.8 X 10(6) U of penicillin G in the treatment of uncomplicated gonococcal urethritis was assessed in a randomized prospective study. Sixty-five evaluable patients received piperacillin, and 55 received penicillin G. All patients received either therapy were cured of gonorrhea. We conclude that piperacillin is as efficacious as aqueous procaine penicillin G in the therapy of uncomplicated gonococcal urethritis.
Gonorrhea↗
Tracheal mucosal damage after aspiration. A scanning electron Microscope study.
Aspiration of gastric contents causes severe pneumonitis, but the effects of such aspiration on the large airways have not been well studied. To evaluate the effects of gastric contents on the tracheal mucosa, 63 healthy A/J mice were anesthetized and aspirated either sterile saline (pH, 5.9) (Group I), hydrochloric acid (pH, 1.5) (Group II), canine gastric juice (pH, 1.5) (Group III), or canine gastric juice (pH, 5.9) (Group IV). Tracer studies showed that the average amount aspirated was 15% of the administered dose. Animals from each group were killed by cervical dislocation at 1, 6, 24, 48, and 72 h and 7 days after aspiration. Examination of the tracheas by scanning electron microscopy revealed normal mucosa in all Group I animals. Tracheas from Group II animals killed between 6 and 48 h after aspiration showed desquamation of the superficial cell layer with complete loss of ciliated and nonciliated cells. Regeneration was noted at 3 days with complete recovery by 7 days. Tracheas from Group III animals had similar changes but regeneration was delayed, whereas those from Group IV had mild desquamation with delayed regeneration. The lungs of group I animals were normal, and those of animals in Group II through IV showed only small widely separated areas of inflammation. We conclude that (1) gastric contents cause marked damage to the tracheal mucosa even when the amount aspirated is too small to induce a clinically significant pneumonia, (2) damage is more severe when the pH of the gastric content is low, and (3) gastric juice may contain substances that delay healing.
Animals↗
Adherence of Pseudomonas aeruginosa to the injured cornea: a step in the pathogenesis of corneal infections.
Keratitis caused by Pseudomonas aeruginosa usually occurs in the setting of corneal injury. This investigation was carried out to ascertain whether injury predisposes to infection by permitting this organism to adhere to the cornea. P. aeruginosa was found to adhere to injured corneas in preference to uninjured ones. Adherence was not immediate and required that the organisms remain on the corneal surface for some time. The number of adhering bacteria appeared to increase with the time the bacteria were allowed to remain on the corneal surface. Use of inocula concentrations of 10(7) to 10(9) was best for studying this phenomenon quantitatively and by microscopy. We conclude that injury allows Ps. aeruginosa to adhere to the corneal surface and suggest that this is the explanation for the clinical observation of a relationship between corneal and injury and Pseudomonas keratitis.
Adhesiveness↗
Fatal influenzal pneumonia in pregnancy: Failure to demonstrate transplacental transmission of influenza virus.
Explore the source record for details and available documents.
Adult↗
Adherence of Pseudomonas aeruginosa to tracheal cells injured by influenza infection or by endotracheal intubation.
Adherence of Pseudomonas aeruginosa to normal, injured, and regenerating tracheal mucosa was examined by scanning electron microscopy. Uninfected and influenza-infected murine tracheas were exposed to six strains of P. aeruginosa isolated from human sources and one strain of platn origin. All of the strains tested adhered to desquamating cells of the infected tracheas, but not to normal mucosa, the basal cell layer, or the regenerating epithelium. Adherence increased when the incubation time of the bacteria with the trachea was prolonged. Strains isolated from human tracheas appeared to adhere better than strains derived from the urinary tract. After endotracheal intubation of ferrets, P. aeruginosa adhered only to the injured cells and to areas of exposed basement membrane. We call this phenomenon "opportunistic adherence" and propose that alteration of the cell surfaces or cell injury facilitates the adherence of this bacterium and that adherence to injured cells may be a key to the pathogenesis of opportunistic Pseudomonas infections.
Animals↗
Outcome of influenza infection: effect of site of initial infection and heterotypic immunity.
An infection established throughout the total respiratory tract of mice with a highly lung adapted influenza virus (H0N1) led to death from viral pneumonia. The 50% lethal dose (LD(50)) was approximately the same as the 50% infectious dose (ID(50)). An infection with the same virus initiated in the nasal mucosa spread to the trachea and lungs over a 3- to 5-day period but was not lethal except at very high infecting doses. The LD(50) was 30,000 times the ID(50). Mice that had recovered from a prior infection with A/PC/73(H3N2) demonstrated enhanced recovery (heterotypic immunity) when challenged with A/PR/8/34(H0N1). Heterotypically immune mice infected while anesthetized with this potentially lethal virus stopped shedding virus from the nose, trachea, and lungs by day 7 and recovered. Heterotypically immune mice, infected awake, stopped shedding virus from the nose by day 5, and, in fact, the virus did not spread to the trachea or lungs. Thus, some of the variation in the severity of influenza infections may be explained by two factors: the site of initial infection and previous infection with heterotypic influenza virus.
Anesthesia↗
Serum antibody prevents lethal murine influenza pneumonitis but not tracheitis.
This paper reports studies showing the effects of serum antibody upon influenza infection at two different sites: the trachea and lung. Tracheal desquamation, pulmonary consolidation, death, and virus shedding were examined after infection of mice with a lethal A/Port Chalmers/1/73 (H3N2) influenza virus. Immune serum administered intraperitoneally before infection prevented death and pulmonary consolidation and also significantly lowered lung virus shedding as compared with controls receiving normal serum. However, this protection did not extend to the ciliated epithelium of the trachea because serum antibody did not prevent desquamation of the trachea or significantly decrease viral yield from the trachea. These results indicate that serum antibody is protective against severe pulmonary parenchymal disease but not for disease of the ciliated epithelium.
Animals↗
Murine influenzal tracheitis: a model for the study of influenza and tracheal epithelial repair.
The murine model of influenza virus infection is generally a lethal pneumonitis produced by a highly mouse-adapted virus. However, we infected mice with a less adapted virus and produced a nonlethal disease that involved the airways without producing gross pneumonitis. Changes that occurred in the tracheal epithelium were studied by scanning and transmission electron microscopy. Complete desquamation of the epithelium occurred within 3 days after infection, regeneration began within 5 days, and repair was complete within 2 wk after infection. This model is proposed as an alternative to the lethal pneumonitis for the study of murine influenza and also as a model for the study of repair of the respiratory ciliated epithelium.
Animals↗
Rocky Mountain spotted fever and jaundice. Two consecutive cases acquired in Florida and a review of the literature on this complication.
Rocky mountain spotted fever is increasing in Florida, a state that has had few cases in the past. The typical clinical illness has been well described, but jaundice has been rarely reported. In two patients with illnesses resembling leptospirosis, jaundice appeared on the sixth and ninth day of illness, and peak bilirubin levels were between 7 and 9 mg/100 ml. Liver biopsy specimen from one patient showed a nonspecific hepatitis. Hemolysis and renal dysfunction may have contributed to the production of jaundice in these patients. Fourteen instances of jaundice were reported in 43 autopsied cases as of 1941, but since that time only rare mention of jaundice has been made.
Child↗
Why is Pseudomonas the colonizer and why does it persist?
Pseudomonas aeruginosa is currently the major cause of morbidity and mortality in cystic fibrosis. Studies to understand why this particular organism is a problem and why host defenses fail to clear it, are beginning to provide some answers. Implicit in any working hypothesis are the prerequisites that: (i) P. aeruginosa should have a tropism for the respiratory tract; (ii) there should be a physical clearance defect; and (iii) there should be an acquired immune clearance defect. Studies from many laboratories support these contentions. This organism exhibits its tropism by adhering to tracheal cells and to tracheobronchial mucins by means of pili or the mucoid exopolysacharide of mucoid strains. The receptors on both cells and mucins contain sialic acid as the dominant sugar moiety. Many factors contribute to its persistence, chief among which is the failure of phagocytic defenses caused by microbial or host enzymes and even by mucins which inhibit the opsonophagocytosis of P. aeruginosa. Injury to the mucociliary system, again caused by microbial or host factors, is also a prominent factor in the persistence of P. aeruginosa. We hypothesize that this organism is the dominant pathogen because of the existence of receptors in the respiratory tract for it and that it persists because bacteria in stagnant mucus cannot be cleared physically or immunologically. We are doubtful that conventional vaccination approaches will yield a solution to this problem.
Bacterial Adhesion↗
The role of bacterial adhesion in cystic fibrosis including the staphylococcal aspect.
The bacteriology of cystic fibrosis shows a unique and predictable progression of colonizing micro-organisms. The reason for this sequence is still not known, but thought must be given to the idea that it may be related to the genetic disorder in some way. If this were to be true, an understanding of the colonization mechanisms at all stages in this progression could provide valuable insights for the development of novel therapies. As far as can be ascertained from published studies, mucus is the site of colonization in cystic fibrosis. While there is no doubt that the major pathogen, Pseudomonas aeruginosa, adheres to injured cells more avidly than to intact cells, the overwhelming evidence indicates that it also attaches more avidly to mucus than to intact airway cells by means of specific adhesin-receptor mechanisms. Studies with Staphylococcus aureus, the other major pathogen, are also in progress. These indicate that this organism also has an affinity for mucus. At this time the studies suggest a lesser affinity than P. aeruginosa, at least with adult mucins. These two organisms do not however appear to share the same receptor. In addition to these two major pathogens, Haemophilus influenzae and Streptococcus pneumoniae, pathogens of lesser importance also adhere to mucus. Therefore adhesion to mucus or mucins may be a recurring theme in all airway colonization. A knowledge of the factors which control these tropisms ought to provide insights into the bacterial specificity seen in cystic fibrosis and other diseases.
Animals↗
Malignant external otitis: report on therapy with ceftazidime and review of therapy and prognosis.
We report the treatment of 20 patients with malignant external otitis (MEO) since 1980. Ceftazidime was used in 15 patients, with cure achieved in 11 of 12 evaluatable patients. An aminoglycoside and an antipseudomonal penicillin were used in five patients, four of whom were cured. The presentation, radiographic studies, therapy, outcome, and period of follow-up in the 20 patients are reported. The previously reported cases of MEO are also reviewed, with a focus on the changing therapy and prognosis. The frequencies of diabetes mellitus, cranial nerve deficits, and treatment failures in MEO have all declined significantly since 1985 from frequencies in earlier years. We conclude that there has been an overall improvement in the diagnosis and treatment of MEO and that monotherapy with ceftazidime shows promise against this potentially fatal pseudomonal infection.
Adult↗
Acinetobacter calcoaceticus variety anitratus: an increasing nosocomial problem.
Acinetobacter calcoaceticus var anitratus is an increasing nosocomial problem in some institutions. Duirng a recent 16-month period, we observed 15 patients with blood isolates of this organism. Thirteen of these patients acquired the organism from the hospital environment. Eleven of these represented real disease and concurrent growth of the organism from another site was predictive of infection (P less than 0.03). A review of laboratory records showed that there was a three-fold increase in nonblood isolates of this organism from hospitalized patients in 1975 and 1976, as compared to 1972 (P less than 0.0001), and a marked seasonal effect was noted, with increased isolations during the summer. Aminoglycoside resistance had increased considerably with 25% of nonblood isolates being resistant to gentamicin and 16% resistant to tobramycin despite its restriction; blood isolates were uniformly susceptible to gentamicin and tobramycin. Reporting of A anitratus as a nosocomial pathogen and serotyping of isolates may be useful to further define its role in nosocomial infections.
Acinetobacter Infections↗
Ceftazidime review.
The chemistry, in vitro activity, adverse effects, and clinical indications for the new third-generation cephalosporin, ceftazidime, are reviewed. Ceftazidime appears to have a unique place among the third-generation agents in the treatment of some infectious processes caused by Pseudomonas aeruginosa. It does not demonstrate superiority to other third-generation drugs against Enterobacteriaceae, aerobic gram-positive cocci, or anaerobes. It is eliminated renally and is similar to ceftizoxime, cefoperazone, and moxalactam in half-life. Ceftazidime shares the safety profile of most of the cephalosporins, and has not been shown to have an effect on prothrombin or produce the disulfuram reaction seen with moxalactam and cefoperazone. Specific indications for its use are discussed.
Bacteria, Anaerobic↗
A position paper on the treatment of hospital acquired pneumonia (HAP): do we need guidelines?
Explore the source record for details and available documents.
Anti-Bacterial Agents↗