Postoperative infection after placement of myringotomy tubes is common. Surgeons and manufacturers of surgical devices have frequently substituted one material for another in middle ear prostheses without analyzing the interaction of material and infection. Implant material attributes are reviewed. Scanning electron micrographs are presented that demonstrate characteristic surface differences between materials and between the same material of different manufacturers. A preliminary clinical controlled study of the covariance of purulence with silicone vs fluorocarbon tubes demonstrates statistically significant differences. The implications of this information are discussed.
Formalin-inactivated Mycoplasma pneumoniae vaccine was administered subcutaneously or intranasally to hamsters to examine the effect of route of administration on immunogenicity and protective effect. Parenterally administered vaccine in the doses employed induced serum complement-fixing antibody formation, but did not significantly decrease the frequency of pneumonia following challenge with virulent M. pneumoniae. Intranasally instilled vaccine was ineffective in stimulating serum antibody, but did diminish the frequency of experimentally induced pneumonia due to M. pneumoniae. However, a greater degree of resistance was induced by intranasal infection with either wild-type organisms or the ts 640 attenuated mutant of M. pneumoniae.
Biomaterial implants frequently potentiate infections in patients, yet rarely have we considered the interactions between bacteria and biomaterials responsible for this. There is extensive literature concerning suture materials of various types and a few studies comparing porous and solid implants. We have developed a simple, relatively atraumatic model for comparing rates of infection surrounding a biomaterial implant in paired single animal observations. Statistically significant differences between silicone and fluorocarbon implants and between silicone and bioglass implants are demonstrated. The relatively greater rate of infection with silicones is consistent with a previous clinical study. The further use of this model for evaluation of material-surface interfacial effects is proposed.
Virus particles were continuously produced by a cell line (78A1) of rat embryo fibroblasts that had been transformed by the murine sarcoma-leukemia virus complex. Since most of the mature virions were found in the extracellular fluid and were not cell-associated, a measurable quantity of viral ribonucleic acid (RNA) could not be extracted from these cells. Cycloheximide, a protein inhibitor, was successfully used to accumulate viral RNA within the cells. This ribonuclease-sensitive RNA, with a sedimentation coefficient of 71S, had the same base composition as the high molecular weight RNA (S20,X = 71) isolated from purified virions released by the transformed cells.
The distribution ofMycoplasma pneumoniae infection in the respiratory tract and the extent of pulmonary pathology were determined by the site ofdeposition and the number of organisms administered to hamsters. Infection of the upper and lower areas of the respiratory tract occurred when organisms were introduced into both areas by small-particle aerosol (2.3 gm) or by intranasal (i.n.) instillation of a 200-,ul inoculum. In contrast, when organisms were delivered primarily to the upper respiratory tract by large-particle aerosol (8 ,um) or by i.n. instillation of a small volume of inoculum (2 or 20 uld), infection remained
A total of 28 cebus monkeys were inoculated intratracheally or intranasally with 10(6) 50% tissue culture infective doses of A/New Jersey/76 virus or 10(7) 50% tissue culture infective doses of A/Victoria/75 virus, and 8 additional monkeys received sterile allantoic fluid. Each of the animals became infected as evidenced by a serological response and/or shedding of the virus. Of the 10 animals inoculated intratracheally with A/Victoria/75 virus, 8 developed a systemic illness, and pulmonary infiltration was detected by X-ray in 7 of the 8. Administration of A/New Jersey/76 virus intratracheally to 10 monkeys produced a mild systemic illness in 2 animals and an upper respiratory tract illness in 6, but no illness developed in the remaining 2 monkeys; none of the animals developed X-ray evidence of lower respiratory tract disease. Intranasal administration of either virus failed to induce any illness or produced, at most, mild illness confined to the upper respiratory tract. These studies demonstrate that cebus monkeys are susceptible to respiratory tract infection with influenza A viruses and that the development of pulmonary disease is reflected in the appearance of easily recognizable radiological changes.
Knowledge of the pathogenesis of pneumonia due to Mycoplasma pneumoniae has been derived primarily from experimental infection of rodents. As part of an effort to establish a model with a closer resemblance to man, three seronegative, young, adult rhesus monkeys (Macaca mulatta) were inoculated with M. pneumoniae (10(7.4) cfu per animal) by oropharyngeal administration of coarse-particle aerosol. Five to six days after exposure of the animals, cultures obtained from the upper respiratory tract were positive for M. pneumoniae. Each animal subsequently developed a serologic response, as determined by complement fixation, complement-mediated killing, and tetrazolium-reduction inhibition techniques. Infection was subclinical, and serial chest roentgenograms failed to disclose pneumonia throughout the course of infection. Blood cell counts and titers of cold agglutinins remained unchanged. Althought M. pneumoniae was recovered from the upper respiratory tract of two monkeys for 50 days, there was no evidence of transmission of infection to cage-mate controls inoculated with broth.
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