scholarly journals Activation of complement by serum-resistant Neisseria gonorrhoeae. Assembly of the membrane attack complex without subsequent cell death.

1982 ◽  
Vol 156 (4) ◽  
pp. 1235-1249 ◽  
Author(s):  
G R Harriman ◽  
E R Podack ◽  
A I Braude ◽  
L C Corbeil ◽  
A F Esser ◽  
...  
Keyword(s):  
Neisseria Gonorrhoeae ◽  
Resistant Strain ◽  
Membrane Attack Complex ◽  
Electron Microscopic Examination ◽  
Sensitive Strain ◽  
Binding Assays ◽  
Electron Microscopic ◽  
Dose Dependent Fashion ◽  
Normal Human ◽  
Resistant Strains

Interaction of the human complement system in normal human serum (NHS) with serum-resistant and -sensitive Neisseria gonorrhoeae was evaluated to better understand the mechanism of serum-resistance. Complement activity (CH50) was depleted from NHS in a dose-dependent fashion by both serum-resistant and -sensitive N. gonorrhoeae. No detectable CH50 remained in NHS incubated with 10(9) colony-forming units (CFU)/ml serum of either resistant or sensitive strains. When smaller numbers of bacteria were incubated with NHS, lesser, yet comparable, amounts of CH50 were depleted by both resistant and sensitive strains. Hemolytic C2 activity was diminished by 33% in the case of resistant N. gonorrhoeae (10(8) CFU/ml serum) and by 48% in the case of a sensitive strain. No detectable decreases in hemolytic C4 or C7 activities were found with either sensitive or resistant strains at this concentration. Both resistant and sensitive strains activated C1s in NHS. Resistant strains specifically activated 19-21% of radiolabeled C1s in NHS, whereas sensitive strains activated 18-32%. Both resistant and sensitive strains also activated C5 in NHS. In binding assays using radiolabeled C5 and C9 in NHS, resistant and sensitive strains bound comparable amounts of C5 and C9. The number of bound C5 and C9 molecules varied according to the number of bacteria or amount of serum used in the assay. The ratio of C9/C5 bound to a sensitive strain was 6.8, and to a resistant strain was 8.2, suggesting that C5 and C9 were incorporated into membrane attack complexes (MAC). Electron microscopic examination of resistant and sensitive strains incubated with NHS revealed that MAC is bound to the surfaces of the resistant strain as well as the sensitive strain.

Evolution of the phenomenon of drug-resistance. II. Studies of the extracellular and intracellular derivatives of folic acid in relation to resistance to sulphathiazole and growth factor requirements

1960 ◽  
Vol 153 (951) ◽  
pp. 205-219 ◽  
Keyword(s):  
Folic Acid ◽  
Growth Factor ◽  
Resistant Strain ◽  
Sensitive Strain ◽  
Vitamin B ◽  
Intracellular Accumulation ◽  
E Coli ◽  
Dependent Strain ◽  
Resistant Strains ◽  
Derivatives Of

This study is a continuation of the results published previously (Sevag & Ishii 1958). It surveys quantitatively the extracellular and intracellular accumulation of p -aminobenzoic acid (PAB), pteridine, folic acid (FA) and citrovorum factor (CF) of the various sulphathiazole (ST)-sensitive and ST-resistant strains of Escherichia coli grown with and without ST. The altered enzymic activities of the resistant strain with respect to growth factor requirement is also determined. The following observations are made. The utilization of the exogenous PAB by the PAB-dependent strain is followed by the multiplication of cells. These events are followed by the extracellular accumulation of FA first and then CF. This pattern applies to other strains of E. coli and is in accordance with the well-known sequence of steps involved in the synthesis of PAB, pteridine, FA, CF and growth. It is shown that PAB accumulates principally extracellularly, and pteridine principally intracellularly. The synthesis of FA by the resistant strain is at least tenfold more resistant to ST than in the sensitive strain. In the resistant strain there is a greater intracellular than extracellular accumulation of FA and CF. In the sensitive strain this relationship is reversed. The resistant strains are inheritably capable of synthesizing greater amounts of pteridine, FA and CF. The PAB-dependent ST-sensitive strain can utilize a combination of 1-methionine and any of the purines, of 1-methionine alone, or vitamin B 12 alone in place of PAB for a partial or full growth. The related resistant strain, on the other hand, is unable to multiply in the salts-glucose medium with and without PAB. It requires a combination of 1-methionine and glycine for growth which cannot be replaced by any of the factors mentioned above. This requirement of the resistant strain for growth is analyzed as a deficiency of the enzymic transmethylations and transhydroxymethylation involving the function of CF in the resistant strain.

scholarly journals Analysis of rdxA and Involvement of Additional Genes Encoding NAD(P)H Flavin Oxidoreductase (FrxA) and Ferredoxin-Like Protein (FdxB) in Metronidazole Resistance of Helicobacter pylori

2000 ◽  
Vol 44 (8) ◽  
pp. 2133-2142 ◽  
Author(s):  
Dong-Hyeon Kwon ◽  
Fouad A. K. El-Zaatari ◽  
Mototsugu Kato ◽  
Michael S. Osato ◽  
Rita Reddy ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Resistant Strain ◽  
Resistance Mechanisms ◽  
Sensitive Strain ◽  
Metronidazole Resistance ◽  
Genes Encoding ◽  
Resistant Strains ◽  
Flavin Oxidoreductase ◽  
H Pylori

ABSTRACT Metronidazole (Mtz) is a critical ingredient of modern multidrug therapies for Helicobacter pylori infection. Mtz resistance reduces the effectiveness of these combinations. Although null mutations in a rdxA gene that encodes oxygen-insensitive NAD(P)H nitroreductase was reported in Mtz-resistant H. pylori, an intact rdxA gene has also been reported in Mtz-resistant H. pylori, suggesting that additional Mtz resistance mechanisms exist in H. pylori. We explored the nature of Mtz resistance among 544 clinical H. pyloriisolates to clarify the role of rdxA inactivation in Mtz resistance and to identify another gene(s) responsible for Mtz resistance in H. pylori. Mtz resistance was present in 33% (181 of 544) of the clinical isolates. There was marked heterogeneity of resistance, with Mtz MICs ranging from 8 to ≥256 μg/ml.rdxA inactivation resulted in Mtz MICs of up to 32 μg/ml for 6 Mtz-sensitive H. pylori strains and 128 μg/ml for one Mtz-sensitive strain. Single or dual (with rdxA) inactivation of genes that encode ferredoxin-like protein (designatedfdxB) and NAD(P)H flavin oxidoreductase (frxA) also increased the MICs of Mtz for sensitive and resistant strains with low to moderate levels of Mtz resistance. fdxB inactivation resulted in a lower level of resistance than that from rdxAinactivation, whereas frxA inactivation resulted in MICs similar to those seen with rdxA inactivation. Further evidence for involvement of the frxA gene in Mtz resistance included the finding of a naturally inactivated frxA but an intact rdxA in an Mtz-resistant strain, complementation of Mtz sensitivity from an Mtz-sensitive strain to an Mtz-resistant strain or vice versa by use of naturally inactivated or functionalfrxA genes, respectively, and transformation of an Mtz-resistant Escherichia coli strain to an Mtz sensitive strain by a naturally functional frxA gene but not an inactivated frxA gene. These results are consistent with the hypothesis that null mutations in fdxB,frxA, or rdxA may be involved in Mtz resistance.

Synthesis, antitrypanosomal and antimycobacterial activities of coumarinic N-acylhydrazonic derivatives

2020 ◽  
Vol 16 ◽  
Author(s):  
Camila Capelini ◽  
Vitória R. F. Câmara ◽  
José D. Figueroa Villar ◽  
Juliana M. C. Barbosa ◽  
Kelly Salomão ◽  
...  
Keyword(s):  
Resistant Strain ◽  
Sensitive Strain ◽  
Moderate Activity ◽  
Active Compounds ◽  
Meaningful Activity ◽  
The World ◽  
Resistant Strains ◽  
Vitro Effect ◽  
Tuberculosis Activity

Background: Near to 5-7 million people are infected with T. cruzi in the world, and about 10,000 people per year die of problems associated to this disease. Method: We reported herein the synthesis, antitrypanosomal and antimycobacterial activities of seventeen coumarinic N-acylhydrazonic derivatives. Results: These compounds were synthesized using methodology with reactions global yields ranging from 46%-70%. T. cruzi in vitro effect were evaluated against trypomastigote and amastigote forms and M. tuberculosis activity were towards H37Rv sensitive strain and resistant strains. Discussion: Against T. cruzi, the more active compounds revealed only moderate activity IC50/96h~20 µM for both trypomastigotes and amastigotes intracellular forms. (E)-2-oxo-N'-(3,4,5-trimethoxybenzylidene)-2H-chromene-3-carbohydrazide showed meaningful activity in INH resistant/RIP resistant strain. Conclusion: These compound acting as multitarget could be good leads for the development of new trypanocidal and bactericidal agents.

In Vitro Activities of StrychnosAlkaloids and Extracts against Plasmodium falciparum

1999 ◽  
Vol 43 (9) ◽  
pp. 2328-2331 ◽  
Author(s):  
Michel Frederich ◽  
Marie-Pierre Hayette ◽  
Monique Tits ◽  
Patrick De Mol ◽  
Luc Angenot
Keyword(s):  
Plasmodium Falciparum ◽  
Resistant Strain ◽  
Inhibitory Concentration ◽  
Sensitive Strain ◽  
Resistant Strains

ABSTRACT The in vitro antimalarial activities of 46 alkaloids and extracts from Strychnos species were evaluated. Two types of quasidimeric alkaloids exhibit high and selective activities againstPlasmodium. Strychnopentamine and isostrychnopentamine were active against chloroquine-sensitive and -resistant strains (50% inhibitory concentration [IC50] ≈ 0.15 μM), while dihydrousambarensine exhibited a 30-fold higher activity against the chloroquine-resistant strain (IC50 = 0.03 μM) than it did against the chloroquine-sensitive strain.

scholarly journals Why sensitive bacteria are resistant to hospital infection control

2017 ◽  
Vol 2 ◽  
pp. 16 ◽  
Author(s):  
Esther van Kleef ◽  
Nantasit Luangasanatip ◽  
Marc J Bonten ◽  
Ben S. Cooper
Keyword(s):  
Hand Hygiene ◽  
Infection Control ◽  
Resistant Strain ◽  
Mechanistic Model ◽  
Antibiotic Use ◽  
Sensitive Strain ◽  
Control Measures ◽  
Infection Control Measures ◽  
Hospital Infection Control ◽  
Resistant Strains

Background: Large reductions in the incidence of antibiotic-resistant strains of Staphylococcus aureus and Clostridium difficile have been observed in response to multifaceted hospital-based interventions. Reductions in antibiotic-sensitive strains have been smaller or non-existent. It has been argued that since infection control measures, such as hand hygiene, should affect resistant and sensitive strains equally, observed changes must have largely resulted from other factors, including changes in antibiotic use. We used a mathematical model to test the validity of this reasoning. Methods: We developed a mechanistic model of resistant and sensitive strains in a hospital and its catchment area. We assumed the resistant strain had a competitive advantage in the hospital and the sensitive strain an advantage in the community. We simulated a hospital hand hygiene intervention that directly affected resistant and sensitive strains equally. The annual incidence rate ratio (IRR) associated with the intervention was calculated for hospital- and community-acquired infections of both strains. Results: For the resistant strain, there were large reductions in hospital-acquired infections (0.1 ≤ IRR ≤ 0.6) and smaller reductions in community-acquired infections (0.2 ≤ IRR ≤  0.9). These reductions increased in line with increasing importance of nosocomial transmission of the strain. For the sensitive strain, reductions in hospital acquisitions were much smaller (0.6 ≤ IRR ≤ 0.9), while communityacquisitions could increase or decrease (0.9 ≤ IRR ≤ 1.2). The greater the importance of the community environment for the transmission of the sensitive strain, the smaller the reductions. Conclusions: Counter-intuitively, infection control interventions, including hand hygiene, can have strikingly discordant effects on resistant and sensitive strains even though they target them equally, following differences in their adaptation to hospital and community-based transmission. Observed lack of effectiveness of control measures for sensitive strains does not provide evidence that infection control interventions have been ineffective in reducing resistant strains.

An ultrastructural morphometric analysis of platelet giant and fusion granules in control subjects and patients with neoplastic myeloproliferative disorders

1983 ◽  
Vol 41 ◽  
pp. 786-787
Author(s):  
Claire M. Payne ◽  
Lewis Glasser
Keyword(s):  
Human Platelet ◽  
Electron Microscopic Examination ◽  
Myeloproliferative Disorders ◽  
Qualitative Assessment ◽  
Structural Elements ◽  
Cell Organelles ◽  
Electron Microscopic ◽  
Platelet Factor ◽  
Normal Human ◽  
Myelomonocytic Leukemia

Electron microscopy has made a significant contribution to our understanding of the normal and defective human platelet. The normal human platelet is ultrastructurally complex and although only 2-4 microns in diameter, contains many cell organelles and structural elements shared with muscle cells and neurons. Platelet organelles include mitochondria, microfilaments, microtubules, α-granules (contain fibrinogen and platelet factor 4), dense bodies (contain serotonin, ADP, ATP and calcium), a dense tubular system and open canalicular system (Fig. 1). An ultrastructural description of giant granules were first reported in 1960 in Willebrand-Jürgens disease. Fusion granules (giant, irregularly-shaped granules) resulting from an apparent "fusion of normal-sized α-granules have since been reported to be characteristic of platelets obtained from patients with preleukemia and myelomonocytic leukemia.Electron microscopic examination of normal platelets in our laboratory revealed occasional granules which also appear fused and irregular in shape.A qualitative assessment of what constitutes an abnormal granule is therefore subjective. The purpose of this study was to establish morphometric criteria which can be used to define the pathological nature of giant and fusion-type platelet granules, and to determine if patients with neoplastic myeloproliferative disorders can be distinguished from patients with a variety of benign conditions for diagnostic purposes.

THE COMPLEMENT-DEPENDENT BACTERIOLYTIC ACTIVITY OF NORMAL HUMAN SERUM: II. CELL WALL COMPOSITION OF SENSITIVE AND RESISTANT STRAINS

1963 ◽  
Vol 9 (1) ◽  
pp. 41-52 ◽  
Author(s):  
A. C. Wardlaw
Keyword(s):  
Cell Wall ◽  
Human Serum ◽  
Resistant Strain ◽  
Cell Walls ◽  
Sensitive Strain ◽  
Normal Human Serum ◽  
Serum Factors ◽  
Rough Strain ◽  
Normal Human ◽  
Smooth Strain

A comparative study has been made of the chemical composition of cell walls from two strains of Escherichia coli—one rough strain which was very sensitive to killing and lysis by normal human serum, and one smooth strain which was relatively insensitive to killing and was not lysed at all. The major components in the cell walls of both strains were protein and (or) polypeptide (70–80%) and lipid (14%), no significant differences in either component being detected between the two strains. A marked difference was, however, detected in the lipopolysaccharide fraction which was present to the extent of only 1% in the walls of the rough, serum-sensitive strain and 9% in the smooth, serum-resistant strain. Moreover, the two lipopolysaccharides were qualitatively different in sugar composition, that from the resistant strain yielding glucose, galactose, rhamnose, and two minor sugar components, while that from the sensitive strain yielded glucose only. These findings are discussed in relation to the three-layer theory for the structure of the coli cell wall and in relation to the serum factors (antibody, properdin, complement, and lysozyme) which may participate in the destruction of bacteria by serum.

scholarly journals Why sensitive bacteria are resistant to hospital infection control

2017 ◽  
Vol 2 ◽  
pp. 16 ◽  
Author(s):  
Esther van Kleef ◽  
Nantasit Luangasanatip ◽  
Marc J Bonten ◽  
Ben S. Cooper
Keyword(s):  
Hand Hygiene ◽  
Infection Control ◽  
Resistant Strain ◽  
Mechanistic Model ◽  
Antibiotic Use ◽  
Sensitive Strain ◽  
Control Measures ◽  
Infection Control Measures ◽  
Hospital Infection Control ◽  
Resistant Strains

Background: Large reductions in the incidence of antibiotic-resistant strains of Staphylococcus aureus and Clostridium difficile have been observed in response to multifaceted hospital-based interventions. Reductions in antibiotic-sensitive strains have been smaller or non-existent. It has been argued that since infection control measures, such as hand hygiene, should affect resistant and sensitive strains equally, observed changes must have largely resulted from other factors, including changes in antibiotic use. We used a mathematical model to test the validity of this reasoning. Methods: We developed a mechanistic model of resistant and sensitive strains in a hospital and its catchment area. We assumed the resistant strain had a competitive advantage in the hospital and the sensitive strain an advantage in the community. We simulated a hospital hand hygiene intervention that directly affected resistant and sensitive strains equally. The annual incidence rate ratio (IRR) associated with the intervention was calculated for hospital- and community-acquired infections of both strains. Results: For the resistant strain, there were large reductions in hospital-acquired infections (0.1 ≤ IRR ≤ 0.6) and smaller reductions in community-acquired infections (0.2 ≤ IRR ≤ 0.9). These reductions increased in line with increasing importance of nosocomial transmission of the strain. For the sensitive strain, reductions in hospital acquisitions were much smaller (0.6 ≤ IRR ≤ 0.9), while community acquisitions could increase or decrease (0.9 ≤ IRR ≤ 1.2). The greater the importance of the community environment for the transmission of the sensitive strain, the smaller the reductions. Conclusions: Counter-intuitively, infection control interventions, including hand hygiene, can have strikingly discordant effects on resistant and sensitive strains even though they target them equally. This follows from differences in their adaptation to hospital- and community-based transmission. Observed lack of effectiveness of control measures for sensitive strains does not provide evidence that infection control interventions have been ineffective in reducing resistant strains.

Immunity in trypanosomiasis

Parasitology ◽  
1959 ◽  
Vol 49 (1-2) ◽  
pp. 143-152 ◽  
Author(s):  
M. A. Soltys
Keyword(s):  
Resistant Strain ◽  
Therapeutic Dose ◽  
Sensitive Strain ◽  
Drug Resistant ◽  
Chemotherapeutic Drugs ◽  
Natural Conditions ◽  
Resistant Strains ◽  
Drug Resistant Strains

Antibody-resistant strains are less sensitive to suramin and antrycide than antibody-sensitive strains. When living trypanosomes were exposed to suramin and antrycide in vitro, antibody-resistant strains needed 50 times more drugs than antibody-sensitive trypanosomes in order to make them non-infectious to mice. In therapeutic experiments in mice the minimal therapeutic dose of drugs for antibody-sensitive strains was 0·1 mg. but for resistant strains it was 0·3 mg./20 g. mice. Rabbits treated prophylactically with suramin resisted infection with the antibody-sensitive strain for a period of 4 months, but failed to resist infection with the antibody-resistant strain after 2 months.Rabbits treated prophylactically with antrycide pro-salt, resisted infection with antibody-sensitive strains for a period of 2 months, but failed to resist infection with the antibody-resistant strain even 1 month after injection with the drug. Although trypanosomes can become drug resistant without being antibody resistant it is suggested that, under natural conditions, drug-resistant strains in animals and man develop from antibody-resistant strains, particularly when trypanostatic drugs are used. It is suggested in conclusion from these experiments that strains of trypanosomes which are exposed for some time to antibodies and become antibody resistant after passage through animals like rabbits, as well as those strains frequently passaged through mice, should be used in all tests for the efficiency of chemotherapeutic drugs.

The Effect of Bovine Lung Heparin on Normal Human Platelets as Measured by Electronic Particle Size Analysis

1982 ◽  
Vol 47 (01) ◽  
pp. 005-007 ◽  
Author(s):  
Margaret R McLean ◽  
Lawrence L Hause
Keyword(s):  
Particle Size ◽  
Microscopic Examination ◽  
Platelet Rich Plasma ◽  
Electron Microscopic Examination ◽  
Particle Size Analysis ◽  
Human Platelets ◽  
Size Analysis ◽  
Electron Microscopic ◽  
Before And After ◽  
Normal Human

SummaryThe response of normal human platelets to treatment with bovine lung heparin was evaluated using electronic particle size analysis and aggregometry. Samples for electronic particle size analysis were obtained both before and after the addition of heparin to platelet-rich plasma (PRP). The number of single platelets decreased significantly after the addition of heparin to PRP obtained from 22 individuals. This decrease averaged 18% in 19 samples which did not show a significant increase in transmittance and was at least 70% in 3 samples which showed a significant increase in transmittance. The size distribution of single platelets was not significantly altered. In addition, electron microscopic examination revealed that platelets treated with heparin are activated.

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