Tinnitus amplification: the high frequency hearing aid.
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Biomedical subjects
Publications and source records attributed to M H Miller.
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We reviewed 56 cases of infective endocarditis (IE) in patients 65 years of age and older. The clinical features, laboratory manifestations, and bacterial etiology of IE in our patients were similar to those in younger patients. Ninety-three percent were febrile, 86% had heart murmurs, and 36% had peripheral stigmas. Streptococci were predominant in community-acquired cases and staphylococci in nosocomial infections; most patients (89%) had persistent bacteremia. Preexisting valvulitis was present in only 23% of patients; 34% had evidence of atherosclerotic heart disease. Complications included congestive heart failure (CHF) in 64%, neurologic sequelae in 36%, and myocardial infarction in 13%. The mortality rate was 45%. A significantly increased mortality was associated with neurologic sequelae, myocardial infarction, or IE with Staphylococcus aureus. The diagnosis of IE should be considered in any elderly patient with a fever, heart murmur, worsening CHF, or an acute cerebrovascular insult.
Gentamicin uptake and killing were studied in aminoglycoside-susceptible wild-type Staphylococcus aureus strains and aminoglycoside-resistant small-colony mutants selected by gentamicin from these strains. In wild-type S. aureus three phases of gentamicin accumulation were noted, and killing occurred during the last and most rapid phase of uptake. Uptake and killing were abolished by anaerobic growth and sodium azide, suggesting that energy-dependent active drug transport required respiration. Treatment of wild-type strains with the uncouplers N,N'-dicyclohexyl carbodiimide (DCCD) and carbonyl cyanide-m-chlorophenyl hydrazone showed disparate effects on gentamicin uptake, producing enhanced and diminished accumulations, respectively. Small-colony mutants demonstrated markedly deficient uptake compared with the wild-type strains and were not killed by gentamicin in concentrations up to 10 mug/ml. Several classes of aminoglycoside-resistant mutant strains are described. One mutant strain was a menadione auxotroph which, when grown in the presence of menadione, exhibited normal gentamicin uptake and killing. Gentamicin uptake and killing in this strain were abolished by KCN when the strain was grown in a medium supplemented with menadione. The membrane adenosine triphosphatase inhibitor DCCD was lethal for this mutant but not for other mutants or wild-type strains. Preincubation with menadione prevented the lethal effect of DCCD, and this strain demonstrated normal gentamicin accumulation when exposed to both DCCD and menadione. A second mutant strain demonstrated both gentamicin uptake and killing in the presence but not the absence of DCCD. Studies with small-colony mutants of S. aureus indicated that the defect in aminoglycoside uptake is very likely related to an inability to generate or maintain energized membranes from respiration. These studies suggest that the membrane energization associated with active aminoglycoside accumulation requires electron transport for the generation of a protonmotive force.
The use of photograms provides a permanent record of microbiological assays in which diffusion of a substance in agar is measured. The accuracy of this procedure is comparable to direct measurement. This technique is inexpensive, does not require special photographic equipment, and is applicable to many tests commonly employed in clinical microbiology and immunology laboratories.
A case of noninfectious arthritis was associated with meningococcal meningitis. Elevated levels of immune complexes were demonstrated in both serum and synovial fluid by the C1q binding assay and Raji cell assay. We believe this complication of meningococcal infection is another disorder in which immune complexes may play a pathogenic role.
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The efficacy of nafcillin and gentamicin used alone and in combination at doses giving serum concentrations comparable to those achieved in patients was studied in rabbits with experimental Staphylococcus aureus endocarditis. The organism used was a penicillinase-producing, methicillin-susceptible, clinical isolate. The addition of gentamicin to nafcillin significantly increased the rate of killing of organisms in valvular vegetations, compared to the effect of nafcillin alone. Gentamicin alone delayed mortality but was not effective in reducing the bacterial populations of the vegetations. Bacteremia persisted in the animals treated with gentamicin alone, in contrast to the groups treated with nafcillin or the combination. Selection of a subpopulation of aminoglycoside-resistant small-colony variants occurred in animals treated with gentamicin alone. This variant was subsequently employed in the rabbit model and produced endocarditis, metastatic infection, and bacteremia comparable to those caused by the parent strain. Animals with infection produced by the variant died later than animals infected by the parent strain. Nafcillin was equally effective in reducing the population of both parent and variant strains in vitro and in therapy of the infected animals. Population studies showed the variant to be a mutant emerging at a rate of 1.9 x 10(-7). It was shown to differ from the parent strain in coagulase and hemolysin production, colonial morphology, and aminoglycoside susceptibility, but was similar by light and electron microscopy and in phage type, pigmentation of colonies, deoxyribonuclease production, mannitol fermentation, and growth rate.
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While intracranial tuberculomas have become uncommon in industrial nations, 12 patients with signs and symptoms of an intracranial mass lesion were recently found to have tuberculomas. Clinical findings suggestive of tuberculosis were frequently subtle or absent. Five patients did not have extracranial tuberculosis. Two patients had intracranial tuberculomas that became superinfected with bacteria and appeared initially as pyogenic brain abscesses. Intracranial tuberculomas in this country almost always occur in adults and represent reactivation of dormant infection. Medical therapy alone is indicated as the initial therapy except in the presence of intolerably increased intracranial pressure. A chemotherapeutic regimen is suggested.
Bacterial sepsis, a major complication of chronic hemodialysis, is due mainly to infections of the vascular access site despite increasing use of internal fistulas. Sixty episodes of septicemia occurred in two chronic dialysis centers, with an incidence of 0.15 episodes of significant bacteremia per patient-dialysis-year in each. Forty-four of the 60 episodes were judged to be due to vascular access site infection by clinical, bacteriologic, and histologic criteria. Seventy percent (31 of 44) of the vascular access site-related episodes were due to staphylococci and 25% (11 of 44) to Gram-negative bacilli; nonvascular access site-related episodes were often due to transplant site infections caused by Gram-negative bacilli or streptococci. Mortality was about 18% in both vascular access site-related and nonrelated septic episodes. Bovine heterograft arteriovenous fistulas more often led to sepsis than did Brescia arteriovenous fistulas. Treatment with appropriate antibiotics was successful in most cases. Routine removal or ligation of the vascular access site was not necessary.
Ocular penetration of 5-fluorocytosine (5FC) was studied in uninfected rabbits after subconjunctival and oral administration. With oral administration, 5FC achieved therapeutic levels in both the vitreous and aqueous humors. The use of a pharmacokinetic model permitted objective comparison of kinetic events within the eye chambers and the serum. The rates of entry and elimination in the vitreous were found to be slower than those in the aqueous, but the mean concentration over 24 hr was the same. The therapeutic levels achieved in the aqueous after subconjunctival administration were of shorter duration, and no detectable levels occurred in the vitreous. Oral administration is clearly therapeutically superior to subconjunctival administration in this model.
Angiography is useful in following selected patients with chemodectoma of the head and neck treated by radiotherapy. Comparison of preradiotherapy and post radiotherapy angiograms in three patients revealed a decrease in the following: size of feeding arteries, size of tumor, intensity of tumor opacification, and degree of venous shunting. When chemodectomas are not amenable to physical examination and when the question of radiotherapy complication vs further growth of tumor arises, postradiotheraphy angiography may be of particular value.
Angiographic experience with chemodectomas in 21 patients is reviewed. Arterial supply was identified from the vertebral artery, the internal carotid artery, and branches of the external carotid artery. A striated cephalad extension from a cervical chemodectoma (five patients) is believed to represent arterial supply to tumor in vein. In two patients, internal and external carotid arteriograms did not opacify important arteries originating near the carotid bifurcation. Retrograde filling of sigmoid sinus (four patients), tumor mass in jugular vein (two patients), and arteriovenous shunting (nine patients) were observed during the venous phase. Thorough angiogra phy is essential for evaluation of chemodectomas of the head and neck.
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