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Biomedical subjects

C E Davis

Publications and source records attributed to C E Davis.

At least 145 records · Page 8Linked to original sources
PubMed1985

Tuberculosis. Cause of death in antibiotic era.

A five-year review (1979 to 1983) of 41 patients with active tuberculosis at the time of death was performed to determine the cause of death. Twenty deaths (49 percent) were directly attributed to tuberculosis. Overwhelming tuberculous disease was the cause of death for seven patients, and among them the majority had strikingly low serum levels of albumin. Ten patients died of either massive hemoptysis or respiratory failure. Only two patients died due to progressive drug-resistant disease in an area where drug resistance is common. The majority of patients (21/41; 51 percent) died of common medical problems unrelated to tuberculosis. Eleven patients died from cardiopulmonary disease (five pulmonary emboli, one respiratory failure due to chronic obstructive pulmonary disease, two acute myocardial infarctions, and two primary dysrhythmias). Three deaths were the result of gastrointestinal bleeding, and three patients died as a result of bacterial superinfection. Our data indicate that patients still die of tuberculosis in the era of effective antituberculosis therapy. It is imperative that clinicians are aware that pulmonary emboli, arteriosclerotic heart disease, bacterial superinfection, and gastrointestinal bleeding cause approximately 50 percent of the deaths among patients who have tuberculosis and that prompt recognition and treatment of those diseases might decrease the mortality from tuberculosis.

Adolescent↗
PubMed1984

Ischemic heart disease risk factors and twenty-year mortality in middle-age Evans County black males.

Ischemic heart disease (IHD) risk factors and 20-year mortality rates were studied in middle-aged Evans County black males. We hypothesized, a priori, that blood pressure, cholesterol, and smoking would be predictive of mortality in black males; that black-white differences in mortality would be due to differences in risk factor levels and not risk functions per se; and that social status would be associated with risk factor levels and would be a predictor of mortality. Multivariate analyses of cumulative risk of dying and time to death suggest that the major IHD risk factors are predictors of all-cause and IHD mortality in black males. Black-white differences in risk functions, specifically for cholesterol, were explained by social status: black males and lower social status white males had similar risk functions, different from those of higher social status white males. Black males and lower social status white males had almost identical survival curves, each less favorable than those of higher social status white males.

Adult↗
PubMed1984

Expression in Escherichia coli of cryptic tetracycline resistance genes from bacteroides R plasmids.

The putative clindamycin resistance region of the Bacteroides fragilis R plasmid pBF4 was cloned in the vector R300B in Escherichia coli. This 3.8-kb EcoRI D fragment from pBF4 expressed noninducible tetracycline resistance in E. coli under aerobic but not anaerobic growth conditions. The fragment does not express tetracycline resistance in Bacteroides, a strict anaerobe. The separate tetracycline resistance transfer system in the Bacteroides host strain V479-1 has no homology to the cryptic determinant on pBF4. In addition, this aerobic tetracycline resistance determinant is not homologous to the three major plasmid mediated tetracycline resistance regions found in facultative gram-negative bacteria, represented by R100, RK2, and pBR322. A similar cryptic tetracycline resistance fragment was cloned from pCP1, a separate clindamycin resistance plasmid from Bacteroides that shares homology with the EcoRI D fragment of pBF4. This study identifies cryptic drug resistance determinants in Bacteroides that are expressed when inserted into an aerobically growing organism.

Aerobiosis↗
PubMed1984

Homology between clindamycin resistance plasmids in Bacteroides.

Two different species of clindamycin-resistant Bacteroides were isolated from the same infection. One isolate contained a single 15-kb plasmid (pCP1) which encoded transferable clindamycin resistance. pCP1 appears similar to the Bacteroides clindamycin resistance plasmid pBFTM10 isolated independently by F.P. Tally, D.R. Snydman, M.J. Shimell, and M.H. Malamy (1982, J. Bacteriol. 151, 686-691). The second strain had a 10-kb plasmid (pCP2) but did not transfer resistance. DNA hybridization studies revealed that pCP1 shares a 5-kb region of homology with the B. fragilis R plasmid pBF4 studied by R.A. Welch and F.L. Macrina (1981, J. Bacteriol. 145, 867-872). This region in both plasmids was shown to be bounded by homologous direct repeats and contains the putative clindamycin resistance determinant. pCP1 and pCP2 were found to share extensive homology but sequences homologous to the clindamycin resistance region were missing from pCP2 and found instead in the whole cell DNA of the host strain. These results identify a transposon-like structure on Bacteroides clindamycin resistance plasmids.

Bacteroides fragilis↗
PubMed1984

Plasmid transfer from Escherichia coli to Bacteroides fragilis: differential expression of antibiotic resistance phenotypes.

A unique shuttle plasmid, pDP1, has been constructed to mediate gene transfer between Escherichia coli and the Gram-negative anaerobe Bacteroides fragilis. pDP1 contains the pBR322 replicon and the Bacteroides clindamycin resistance plasmid pCP1 linked to the transfer origin of the broad host range plasmid RK2. pDP1 can be transferred from E. coli to B. fragilis by the RK2 conjugation system even though RK2 itself is not maintained in the Bacteroides recipients. The antibiotic resistance and replication functions of pDP1 have been mapped by deletion analysis, and a 5-kilobase portion of the plasmid has been identified as the essential region for maintenance in Bacteroides. Comparison of the resistance conferred by pDP1 on E. coli and B. fragilis shows that antibiotic resistance genes are expressed differently in aerobic and anaerobic bacteria. These results document the feasibility of gene transfer from E. coli to B. fragilis and demonstrate the usefulness of this conjugation system to study genetic structure and expression in Bacteroides.

Bacteroides fragilis↗
PubMed1984

Genetic resistance to African Trypanosomiasis.

Genetic resistance to African trypanosomiasis occurs in certain breeds of livestock, many species of wildlife, some strains of mice, and possibly humans. The term trypanotolerance is used to describe this trait, which in domestic livestock is best exhibited by the indigenous West African taurine breeds of cattle, N'Dama and West African Shorthorn, that have been in Africa for 5,000 to 7,000 years. Confirmation not only that these breeds are genetically resistant to trypanosomiasis but also that they are at least as productive as other indigenous breeds is currently leading to their increased use in livestock-development projects in tsetse-infested areas. Trypanotolerance appears to be related to the control of parasitemia, a capacity associated with an event that regulates parasite growth and determines how rapidly the immune response is triggered. Identification of the factors that regulate this event and definition of their genetic basis may have important implications for the development of novel strategies for control of African trypanosomiasis.

Anemia↗
PubMed1984

Indomethacin promotes differentiation of Trypanosoma brucei.

The treatment of mice with indomethacin lowered Trypanosoma brucei parasitemia 1 to 2 log10 because it quickly promoted the differentiation of rapidly dividing long, slender trypanosomes into short, stumpy forms that do not divide in the mammal but do develop a functional mitochondrion and the ability to infect the tsetse. Since natural resistance correlates with the rate of differentiation, this observation may provide important information about factors that control the severity of trypanosomiasis.

Animals↗
PubMed1983

Genetic analysis of clindamycin resistance in Bacteroides species.

The genetic basis of clindamycin and tetracycline resistance in species of Bacteroides was studied in 13 resistant clinical isolates; 10 isolates were resistant to high levels of clindamycin (greater than 160 micrograms/ml) and three were resistant to low levels of clindamycin (5-20 micrograms/ml). All of the isolates were resistant to tetracycline. None of the strains with low-level clindamycin resistance could transfer resistance to either antibiotic. Three isolates resistant to high levels of clindamycin transferred tetracycline resistance to a sensitive Bacteroides fragilis recipient, and one of these (strain 1126) also transferred high-level clindamycin resistance. None of the transfer-proficient strains of Bacteroides contained plasmid DNA. However, DNA homology was detected by hybridization between the clindamycin resistance plasmid pBF4 isolated in France and sequences in our high-level clindamycin-resistant strains from California. A common homologous 4.8 megadalton EcoR1 fragment was identified in the whole cell DNA of the transfer-proficient strain 1126 of B. fragilis and two other species of the B. fragilis group.

Bacteroides↗
PubMed1983

Mechanism of action of metronidazole on Bacteroides fragilis.

Metronidazole (10 micrograms/ml) was rapidly bactericidal when added to log-phase cultures of Bacteroides fragilis strain 2624. DNA synthesis stopped immediately after addition of metronidazole, whereas synthesis of RNA and protein continued at linear rates for at least 60 min. Gel electrophoresis of DNA extracted from metronidazole-treated cells revealed no nicking or strand breakage in either the 2.9- or 2.0-megadalton plasmid of strain 2624. Also, no degradation of chromosomal DNA was seen. DNA polymerase activity, measured in vitro, was not diminished by prior treatment of the cells with metronidazole. Thus, the primary action of metronidazole is a rapid inhibition of DNA replication. The DNA remains structurally intact, DNA polymerase activity is not directly affected, and cells retain metabolic activity, synthesizing RNA and protein at unaltered rates.

Bacterial Proteins↗
PubMed1983

Effects of penicillinase on bactericidal and complement activities in normal human serum.

During routine addition of penicillinase (beta-lactamase) to patients sera, we found that the capacity of some of these sera to kill serum-sensitive gram-negative organisms was significantly decreased. Further controlled studies showed that penicillinase decreased both the bactericidal activity of normal human sera and the total hemolytic activity (CH50) of complement in these sera. The decreased bactericidal activity correlated significantly (r = 0.57, P less than 0.05) with the reduction of CH50 in eight normal sera. These effects of penicillinase were time and temperature dependent. Measurement of individual complement component activities showed that penicillinase decreased the activity of C2, C4, and C3-C9, suggesting that the penicillinase preparation activated the classical pathway. These results cast doubts on the validity of bactericidal determinations when sera are pretreated with penicillinase.

Bacteria↗
PubMed1983

Killing of Aspergillus spores depends on the anatomical source of the macrophage.

To resolve the controversy over the capacity of macrophages to kill or inhibit germination of Aspergillus spores, we compared this function in peritoneal and alveolar macrophages. Alveolar macrophages from rabbits killed 82 to 90% and completely digested 72 to 82% of spores of Aspergillus fumigatus in 30 h. In contrast, peritoneal macrophages could not even inhibit the germination of ingested spores; more than 85% transformed into mycelia within 24 h. Killing by alveolar macrophages was delayed for 3 to 6 h after phagocytosis and was independent of oxidative killing mechanisms and immune activation. The ability of alveolar macrophages to kill Aspergillus spores without modulation by T lymphocytes or the generation of oxygen intermediates points out that concepts built on studies of peritoneal macrophages may be misleading and underscores the importance of studying the role of macrophages in immunity with cells from the appropriate anatomical site.

Animals↗
PubMed1983

Models of T cell deficiency in listeriosis: the effects of cortisone and cyclosporin A on normal and nude BALB/c mice.

It is often difficult to test the role of T lymphocytes in resistance to infection because most models of T cell deficiency are associated with altered nonspecific resistance. In an attempt to address this problem, we compared the effects of cyclosporin A (CyA), cortisone (CA), and the athymic state on the course of murine listeriosis. We chose listeriosis because resistance to Listeria monocytogenes occurs in two phases. Bacterial multiplication is controlled by nonspecific defense mechanisms in the early phase and by acquired T cell-dependent immunity in the second phase. Mice treated with CA died during the early phase, probably because of inhibition of the antimicrobial activity of nonimmune macrophages. Accordingly, the immunosuppressive effect of CA was similar in athymic and normal mice. Untreated nude mice developed chronic low grade infection, probably because of heightened activity of nonimmune macrophages. In contrast, immunosuppression with CyA did not affect early resistance but induced overwhelming, fatal disease in the later phase when control mice began to acquire resistance. CyA did not change the course of listeriosis in nude mice, confirming its specificity for T cell-dependent immunity. Thus, this study shows that CyA is a potent and specific inhibitor of T cell-mediated immunity and that T cell-dependent resistance is essential for survival from listeriosis, a conclusion that could not have been established by studies of the nude mouse or immunosuppression by CA.

Animals↗
PubMed1982

The clinical significance of clindamycin-resistant Bacteroides fragilis.

The Bacteroides fragilis group of bacteria are the most numerous microorganisms in the colon and the most common anaerobic isolates from human infections. Although clindamycin hydrochloride is still considered the antibiotic of choice for treatment of infections with these bacteria, resistant strains are becoming more common. To determine the clinical significance of clindamycin-resistant bacteroides, we reviewed the charts of 14 patients with resistant isolates. Clindamycin resistance was a major factor in the clinical course of at least four patients. Three of these did not recover until they were treated with effective antimicrobials. Seven patients had been treated with either erythromycin or clindamycin before isolation of the resistant strain. These observations underscore the importance of antimicrobial sensitivity testing of the B fragilis group and of considering the possibility of resistance when patients infected with Bacteroides fail to respond to clindamycin treatment.

Abdomen↗