Malignant pleural effusions: pleurodesis using a small-bore percutaneous catheter

This study describes our experience using a percutaneously placed small-bore catheter for drainage of malignant pleural effusions and subsequent instillation of a sclerosing agent to obliterate the pleural space. We treated 15 consecutive patients with known metastatic cancer and a symptomatic pleural effusion. Twelve patients survived for more than four weeks after the procedure; 11 of these 12 patients had a successful objective clinical response. The procedure was well tolerated, with little or no discomfort during catheter placement and the maintenance period. No serious complications were encountered. We conclude that the use of a small-bore percutaneously placed "pneumothorax" catheter in the management of malignant pleural effusions is an effective and more comfortable alternative to large-bore closed-tube thoracostomy.     

Confirmation that the Type I collagen gene on chromosome 17 is COL1A1 (α1(I)), using a human genomic probe

A cloned 15 kb genomic fragment from the human α1 (I) collagen gene (COL1A1) has been used as a probe on restriction digests of DNA from human-mouse somatic cell hybrids. Positive results on hybrids containing chromosome 17 as their only karyotypically visible human material confirm the assignment of this gene to chromosome 17. Hybrids which contain fragments of chromosome 17 are used to confirm the localization to 17q21-qter.     

Plasmids of Ewingella americana: supplementary epidemiologic markers in an outbreak of pseudobacteremia.

During an outbreak of pseudobacteremia in a children's hospital, Ewingella americana was found in blood cultures from 20 patients. E. americana was inoculated into blood culture bottles at the time of specimen collection due to cross contamination from nonsterile, citrated blood collection tubes used for coagulation studies. Antimicrobial susceptibility testing and plasmid profiling were used to assess the association between patient isolates and isolates from unused blood collection tubes. All E. americana isolates had similar antibiograms (i.e., resistance only to cephalothin) when tested at 37 degrees C. However, when the same isolates were tested for antimicrobial susceptibility at 25 degrees C, a different antibiogram (i.e., resistance to chloramphenicol, ampicillin, and cephalothin) was found. The majority of these isolates also demonstrated a unique four-plasmid profile (130, 56, 4.6, and 3.1 megadaltons), and two of these plasmids (130 and 56 megadaltons) were characterized as temperature-sensitive plasmids. An epidemiologic link between outbreak-associated isolates obtained from different time periods in the outbreak was supported by evidence of a significant trend in the ability of the outbreak-associated isolates to reduce nitrate, together with the presence of the resistance antibiogram at 25 degrees C and the demonstration of the unique four-plasmid profile.     

Nosocomial Pseudomonas pickettii colonization associated with a contaminated respiratory therapy solution in a special care nursery.

Pseudomonas pickettii caused respiratory tract colonization in five infants in the special care nursery of a Chicago hospital. All organisms had the same antimicrobial susceptibilities. Endotracheal suctioning with saline from 5-ml unit-dose vials was identified by epidemiologic investigation as a risk factor for colonization. The vials of saline were contaminated with a strain of P. pickettii having the same antimicrobial susceptibility pattern as the isolates from patients. As part of an investigation of the manufacturing plant where the saline solution was produced, P. pickettii was recovered from deionized water used to make the product and from several sites in the processing line. Bypassing of a 180 degrees F (ca. 82 degrees C) water-holding tank appeared to be temporally related to product contamination. The ability of P. pickettii to survive and grow in this solution has been demonstrated in the laboratory. This outbreak demonstrates that, despite pertinent Food and Drug Administration regulations and company programs for identifying such contamination, intrinsically contaminated solutions can occasionally reach the bedside of the patient.     

Adherence of Streptococcus pneumoniae to Human Bronchial Epithelial Cells (BEAS-2B)

Pneumococcal adherence to alveolar epithelial cells and nasopharyngeal epithelial cells has been well characterized. However, the interaction of Streptococcus pneumoniae with bronchial epithelial cells has not been studied. We have now shown that pneumococci bind specifically to a human bronchial epithelial cell line (BEAS-2B cells). Pneumococci adhered to BEAS-2B cells in a time- and dose-dependent manner. These results suggest that the bronchial epithelium may serve as an additional site of attachment for pneumococci and demonstrate the utility of the BEAS-2B cell line for studying mechanisms of pneumococcal infection.     

Effect of atropine and vagotomy on response of transplanted pancreas.

It is well established that atropine and vagotomy inhibit pancreatic enzyme secretion in response to intestinal stimulants such as fat or amino acids. These effects are usually attributed to interference with hypothetical vagal cholinergic mechanisms that facilitate release of cholecystokinin. To determine whether atropine or vagotomy interferes with release of humoral stimulants of pancreatic enzyme secretion, we studied their effect on protein secretion from an autotransplanted portion of pancreas in response to intestinal stimulants in dogs. The transplanted pancreas was as sensitive as the intact pancreas to stimulation by exogenous caerulein, a cholecystokinin-like peptide, and this response was not altered by atropine or vagotomy. Therefore, if vagotomy or atropine interferes with release of humoral pancreatic stimulants, they would be expected to reduce the response of the transplanted pancreas just as they do of the intact pancreas. Truncal vagotomy caused no significant change in protein secretion from the transplant in response to intestinal perfusion with sodium oleate or tryptophan. Atropine was tested only against sodium oleate and caused no change in response. We conclude that release of humoral pancreatic excitants of protein secretion in response to intestinal stimulants is not significantly changed by atropine or vagotomy.