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Biomedical subjects

K H Mayer

Publications and source records attributed to K H Mayer.

At least 127 records · Page 7Linked to original sources
PubMed1988

Medical costs of ambulatory patients with AIDS-related complex (ARC) and/or generalized lymphadenopathy syndrome (GLS) related to HIV infection, 1984-85.

A cost-of-illness study July 1, 1984-June 30, 1985 evaluating 28 patients with AIDS-Related Complex (ARC) and/or Generalized Lymphadenopathy Syndrome (GLS) found the average cost to be $489 per patient per year. None of the ARC or GLS patients in our study was hospitalized during the one year period, and none progressed to AIDS. No AIDS-specific treatment such as AZT was available at the time this study was completed.

AIDS-Related Complex↗
PubMed1987

Compulsory premarital screening for the human immunodeficiency virus. Technical and public health considerations.

The effectiveness of a mandatory premarital screening program was examined as a means of curtailing the spread of the human immunodeficiency virus (HIV) infection in the United States. The epidemiology of the HIV, the technical characteristics of tests for antibodies to HIV, and the logistic, economic, and legal implications of such a program were considered. In one year, universal premarital screening in the United States currently would detect fewer than one tenth of 1% of HIV-infected individuals at a cost of substantially more than +100 million. More than 100 infected individuals would be told that they were probably not infected, and there would likely be more than 350 false-positive results. Public education, counseling of individuals, and discretionary testing can be important tools in reducing the spread of HIV infection, but mandatory premarital screening in a population with a low prevalence of infection is a relatively ineffective and inefficient use of resources.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Pharmacokinetics and pharmacodynamics of intravenous ciprofloxacin. Studies in vivo and in an in vitro dynamic model.

The pharmacokinetics and pharmacodynamics of a 200-mg intravenous dose of ciprofloxacin were studied in normal volunteers and in an in vitro dynamic model that exposes bacteria to changing concentrations of the drug in a neutropenic setting. Peak ciprofloxacin concentrations in vivo averaged 3.2 micrograms/ml. The terminal serum elimination half-life averaged 4.2 hours. The volume of distribution of ciprofloxacin was large and consistent with extensive extravascular distribution. Slightly less than half of the dose was recovered unchanged in urine by 48 hours after infusion. The median serum bactericidal titer against a strain of Escherichia coli was 1:16 or more for at least six hours after infusion, but was only 1:2 against a strain of Pseudomonas aeruginosa immediately after the end of the infusion. Pharmacodynamic studies in the in vitro model with a simulated regimen of 200 mg administered intravenously every 12 hours demonstrated rapid and complete killing of this strain of E. coli following the first 200-mg "dose." For the strain of P. aeruginosa, an initial bactericidal effect was observed due to the eradication of susceptible subpopulations of bacteria; however, regrowth of resistant organisms was observed. These data suggest that a regimen of 200 mg administered intravenously every 12 hours results in rapid killing of susceptible bacteria. Higher doses or combination therapy may be required to prevent the emergence of resistant P. aeruginosa in this model and in the setting of neutropenia.

Bacterial Infections↗
PubMed1987

Antibacterial therapy in patients with malignancies.

Patients with malignant disease may be predisposed to bacterial infections because of neoplastic disruption of normal tissue barriers, exogenous immunosuppressive therapy (drugs with or without radiation), and intrinsic host immune deficits secondary to these diseases. Diminished polymorphonuclear leukocyte numbers or function and impaired humoral immunity are highly correlated with the development of serious bacterial infections. The usual signs and symptoms of infection may be absent or altered in a compromised host. Therapy must be instituted promptly upon clinical suspicion of bacterial infection, and empirical choices should usually include combinations that are synergistic for likely pathogens based on knowledge of the local predominant flora and susceptibility data. Synergism has most often been demonstrated in combinations that utilize a beta-lactam (semisynthetic penicillin or cephalosporin) and an aminoglycoside. Triple drug therapy has not been shown to be advantageous. Monotherapy with third generation cephalosporins, carbapenems, monobactams, or ureidopenicillins has not been proven to offer advantages over 2-drug regimens for these patients. Patients with blood deficient in granulocytes (granulocytopenic) who respond to 2-drug therapy but remain deficient in neutrophils (neutropenic) may need continued treatment until the neutropenia subsides. Those who do not respond and remain febrile with an unclear focus of infection may need to be started on antifungal therapy in addition to the antibacterial agent. The use of oral agents for the prophylaxis of neutropenic patients against bacteremia remains controversial. If drugs are used, co-trimoxazole and nystatin suspension may be preferable.

Anti-Bacterial Agents↗
PubMed1987

Correlation of enzyme-linked immunosorbent assays for serum human immunodeficiency virus antigen and antibodies to recombinant viral proteins with subsequent clinical outcomes in a cohort of asymptomatic homosexual men.

A cohort of asymptomatic homosexual men at a Boston community health center was screened for the presence of human immunodeficiency virus (HIV) serum antigen and antibodies to recombinant proteins containing portions of the envelope and the gag (core) gene products. Of 196 asymptomatic men screened, 149 were antigen-negative/antibody-negative, 41 were antigen-negative/antibody-positive, and six were antigen-positive/antibody-positive. All three men in whom the acquired immune deficiency syndrome (AIDS) developed over the next year were antigen-positive at enrollment. Although a larger portion of the men who were antigen-positive and did not demonstrate progression to AIDS after one year had thrush, zoster, or generalized lymphadenopathy, the associations were not statistically significant. Whereas all of the seropositive men had antibody to viral envelope antigens, about a quarter did not have detectable antibodies to recombinant core antigens. However, all of these men had detectable antibody to core antigens by Western blot. Titers to recombinant core and envelope antigens tended to be lower in the men with AIDS. HIV-infected persons who are more likely to have enhanced immuno-compromise may be identified by these newer tests, but further longitudinal studies will be necessary to fully understand their prognostic value.

AIDS-Related Complex↗
PubMed1986

Review of epidemic aminoglycoside resistance worldwide.

Epidemic aminoglycoside resistance may be caused by the spread of a species with distinctive chromosomal genes (e.g., Pseudomonas aeruginosa), or it may be due to the dissemination of plasmids or transposons between genera. Although strains of P. aeruginosa resistant to aminoglycosides because of impermeability may cause nosocomial outbreaks, most of the acute increases in aminoglycoside resistance are due to the spread of inactivating enzymes by plasmids. The index species for intergeneric outbreaks is usually Klebsiella pneumoniae carrying the ANT(2") or AAC(3) gene; however, the distribution of resistance varies greatly by location and species. The AAC(6')-I gene is most common in Serratia marcescens and in East Asian isolates of other species, whereas the AAC(3) gene is common in Chile. In the United States, the ANT(2") and AAC(3) genes are particularly common among Enterobacteriaceae, except for Proteus and Providencia, which often carry the AAC(2') gene. The most common patterns of epidemic resistance lead to the inactivation of gentamicin and, less frequently, tobramycin, but only rarely affect amikacin.

Acetyltransferases↗
PubMed1986

Defective T-cell differentiation in acquired immune deficiency syndrome (AIDS).

A decline in T-cell lymphocyte number is the central characteristic of acquired immune deficiency syndrome (AIDS). The reason for the loss of these cells is not well understood. We investigated the hypothesis that defects in T-cell differentiation contributed to T-cell loss using an in vitro colony assay that measures T-cell precursor (CFU-T) frequency. The results indicate a substantial generalized decrease in CFU-T in people with AIDS (P less than 0.01), most of whom have Kaposi's sarcoma, and an occasionally severe decrease in CFU-T in people with ARC. Some of the cells from low colony formers suppressed colony formation by control cells. In addition, plasma from people with AIDS was less supportive of colony growth than control plasma. Decreased Ia expression on adherent mononuclear cells did not correlate with colony formation. A defect in T-cell repopulation can help explain the loss of T cells associated with AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Association of human T lymphotropic virus type III antibodies with sexual and other behaviors in a cohort of homosexual men from Boston with and without generalized lymphadenopathy.

Forty asymptomatic homosexually active men seen at a Boston community health center and 39 men with generalized lymphadenopathy were interviewed and filled out detailed epidemiologic questionnaires. Twenty percent of the asymptomatic men and 92 percent of those with lymphadenopathy had antibodies to human T lymphotropic virus type III (HTLV-III). None of the men have subsequently had the acquired immune deficiency syndrome (AIDS). Seropositivity was associated with receptive anal intercourse and oral exposure to ejaculate, a history of hepatitis B, anal gonorrhea, or intestinal parasites, but no other sexually transmitted diseases, and did not correlate with the use of recreational drugs. More of the seropositive men had multiple partners from New York City. An association with seropositivity was less evident in relation to the numbers of partners from San Francisco or Los Angeles, since the whole cohort generally had fewer contacts with partners from these cities. The data suggest that educational programs among homosexual men attempting to decrease AIDS risk should focus on decreasing the number of partners, receptive anal intercourse, oral exposure to ejaculate and other intimate rectal contact, and sexual contact with men from areas of increased HTLV-III seroprevalence.

Adult↗
PubMed1986

Recurrent salmonella infection with a single strain in the acquired immunodeficiency syndrome. Confirmation by plasmid fingerprinting.

Five weeks before the development of acquired immunodeficiency syndrome (AIDS), a 38-yr-old homosexual man had symptomatic gastroenteritis that resolved without antibiotic treatment. His stool culture was positive for Salmonella typhimurium at that time. The patient subsequently developed Pneumocystis carinii pneumonia and received a 10-day course of intravenous trimethoprim-sulfamethoxazole. He developed salmonella bacteremia 4 months later. The salmonella isolates from the stool and blood were susceptible to trimethoprim-sulfamethoxazole. Comparison of cryptic plasmids showed a pattern identical to the initial salmonella infection, so infection with a new strain did not cause the bacteremia. This finding illustrates the utility of plasmid fingerprinting as a diagnostic tool, and suggests that persons with AIDS, or those at high risk with prodromal symptoms, should receive prompt, effective therapy for nontyphoidal salmonella gastroenteritis.

Acquired Immunodeficiency Syndrome↗
PubMed1986

The epidemiology of antibiotic resistance in hospitals.

Changes in antibiotic susceptibility among different species are a function of the interaction of bacterial genomes (chromosomes, plasmids, transposons) with specific host and environmental factors. Computer-assisted surveillance of resistance patterns and plasmid fingerprinting with restriction endonucleases have facilitated resistance gene tracking. Certain nosocomial plasmids have persisted for many years within specific centres, others are widely distributed by species and location, and others may have a narrow host range or undergo rapid molecular evolution. Klebsiella pneumoniae is most often the index species for the dissemination of nosocomial plasmids, which are frequently multiresistant. Acute increases in antibiotic resistance may be due to antibiotic selection pressures, introduction of new, well-adapted species, over-crowding and other environmental changes. The most resistant organisms are found in units where patients are immunocompromised, are subject to invasive procedures or remain for long periods. Although large-scale studies have not shown uniform increases in the prevalence of resistant bacteria, acute outbreaks in specific niches have resulted in increased patient morbidity, necessitating rapid changes in antibiotic usage. Further molecular epidemiological studies are required in order to understand better how to anticipate the spread of antibiotic resistance.

Anti-Bacterial Agents↗
PubMed1986

Molecular evolution, species distribution, and clinical consequences of an endemic aminoglycoside resistance plasmid.

During the first 6 years after appearing in one hospital, a 92-kilobase conjugative plasmid, pBWH1, which encoded resistance to chloramphenicol and sulfonamides and determined TEM-1 beta-lactamase and 2''-aminoglycoside nucleotidyltransferase, underwent a variety of molecular changes. It was most prevalent initially in isolates of Klebsiella pneumoniae, then in isolates of Serratia marcescens, and finally, after nearly disappearing, in isolates of Enterobacter cloacae. Evolutionary changes in the plasmid did not account for its shifts in species distribution, since the original molecule was found in isolates of each species. The late resurgence of pBWH1 occurred after a copy of its original molecule entered a distinctive ornithine decarboxylase-negative strain of E. cloacae, new to the hospital. The resulting transconjugant strain, chromosomally resistant to topical silver salts and to cephalosporins, and with the addition of pBWH1-encoded aminoglycoside resistance, spread in the hospital by causing an outbreak of sepsis in the burn unit, where these were commonly used antibacterial agents. Thus, an endemic plasmid became prevalent in a new host species because one of its genes supplemented the fitness of an uncommon strain of the species for a particular clinical niche.

Aminoglycosides↗