Physiology of thermophilic bacteria.
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The mechanism by which interference with the biosynthesis of bacterial cell wall causes death and lysis of bacteria appears more complex than originally thought. In an earlier model of the mode of action of beta-lactams, it was assumed that, in the presence of the antibiotics, bacteria synthesize a mechanically weak (poorly cross-linked) cell wall that ruptured under the osmotic-mechanical pressure of the normally growing cytoplasmic mass. However, recent findings suggest a much more complex picture. Lysis and, in at least some bacteria, loss of viability as well, seem to be catalyzed by autolytic enzymes (murein hydrolases), the destructive activity of which is triggered in the beta-lactam-treated bacterium via a poorly understood mechanism. Furthermore, different species of bacteria respond quite differently to treatment with the same beta-lactam: some bacteria are both killed and lysed, others only lose viability, whereas still other species respond mainly by a reversible inhibition of growth (beta-lactam-tolerant bacteria). In addition, structurally different beta-lactams may cause quite different biochemical, morphological, and antibacterial effects, even within the same bacterial species. It is conceivable, therefore, that there is more than one mechanism for loss of viability and/or lysis. Most of the bacteria examined so far contain a number (four to eight) of different penicillin-binding proteins. Genetic and physiological evidence obtained in E. coli indicate that these proteins play essential roles in a variety of physiological functions, such as maintenance of structural integrity, shape, and cell division. Pneumococci with a suppressed autolytic system are resistant to he lytic (and, partially at least, to the bactericidal) effect of beta-lactams. Interference with cell wall synthesis seems to trigger autolysin activity by upsetting the cellular control of autolytic enzyme. It is suggested that the irreversible antimicrobial effect of beta-lactams may have an indirect mechanism in other bacteria as well.
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Bacteria exhibit varying niche breadths, with generalists thriving in diverse environments and specialists confined to specific habitats. Although genes for cooperative traits have been suggested to influence niche breadth evolution, their precise role remains unclear. We used a combination of phylogeny-based comparative methods to test causal hypotheses about the directionality of the relationship between genes for cooperation and bacterial niche breadth evolution across 25,785 species. Our results revealed 1) a positive correlation between the proportion of genes for cooperation and niche breadth; 2) genes for cooperation influenced niche breadth evolution, with a decreased proportion of such genes promoting niche contraction as the predominant evolutionary direction; and 3) genes for cooperation experience more frequent gain and loss within species rather than across species. These findings suggest a role of bacterial cooperation in influencing niche breadth evolution and maintaining the ecological versatility of bacteria. While our results are consistent with a simple relationship under the hypotheses tested, more complex causal scenarios are possible, including the role of factors that influence both cooperation and niche breadth.
Legionnaires' disease bacterium in tissue does not readily react with the Gram stain but can be seen by other stains and direct immunofluorescence. It is a slow-growing, aerobic, gram-negative rod that can be cultivated over a narrow temperature range on Mueller-Hinton agar supplemented either with complex biological mixtures or certain ferric salts and cysteine. The bacterium produces unique, branched-chain fatty acids, catalase, oxidase (weakly), and gelatinase and uses starch while ignoring other carbohydrates. Pigment production is related to tyrosine in the medium. In-vitro studies suggest susceptibility to all antibiotics except vancomycin, but a class 1 beta-lactamase has been demonstrated. Analysis of DNA confirmed the unrelatedness of this bacterium to previously recognized prokaryotes. Diagnosis of the disease has depended largely on serologic test findings and the demonstration of the bacterium in tissue and, occasionally, on isolation. Additional, simpler, and more rapid diagnostic tests should soon be available.
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A new frame of reference, which in its fundamental structuring differs radically from the structuring of the familiar western Indo-European viewpoints (logical, mathematical, scientific, philosophical, etc.), already exists. Recently, by the strategem of systematically disallowing a previously unnoticed untenable assumption encoded in the traditional Western symbolic logics, set theories, etc., in particular and in the Western 'World-View' in general, this frame of reference has generated its own, entirely non-traditional, formalized language. The Notre Dame Journal of Formal Logic has accepted for publication a first paper presenting this non-standard formalized language (Hilgartner, 1975). As one of its accomplishments, this new frame of reference delivers a general theory of living. This theory purports to span the entire domain of what we call living systems, human or non-human. The author did not originally devise this new frame of reference to account for the observable 'doings' of one-celled organisms. Consequently, any effort to illustrate the generalizations of this already-existing abstract theory in terms of humanly observable bacterial behavior has the effect of experimentally testing these generalizations. In the second portion of this paper, the author shows that the new viewpoint neatly accounts, with no 'loose ends,' for the published observations concerning the sensing of chemicals by bacteria; and also proposes two new experiments. Meanwhile, there exists a special dilemma which arises whenever its adepts attempt to discuss this non-standard frame of reference with persons versed in the standard Western one. By delineating the structuring of this dilemma, in the context of a human studying the sensing of chemicals by bacteria, the author demonstrates that the untenable assumption mentioned above does underlie the traditional Western viewpoints; and this demonstration suffices to show the traditional Western 'World-View' as fundamentally flawed.
An 125I absorptiometry technique is described which has sufficient precision to detect the alveolar bone loss associated with ligature-related periodontitis in the monkey. Six monkeys had significant drops in alveolar bone mass 14 days after the the application of a silk ligature around the gingival margin of an adjacent tooth. Variation in the magnitude of bone loss was observed. These may represent variations in the pathogenicity of the microflora produced in response to a ligature and/or variation in host response to the insult produced by specific dental plaque organisms. The lack of bone loss post-ligature plus antibiotic therapy supports the theory that the bacterial-host interaction, not simply irritation from the ligature alone, is responsible for the bone loss. The potential for bone regeneration after ligature-induced bone loss is demonstrated.
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Twenty-six teeth from 8-month-old beagle dogs were used to evaluate the pulpal response to bacteria in bacterially contaminated minimally exposed and unexposed pulp in the dog. The effects were evaluated by means of serial radiographs, consecutive vital dye injections, and histologic sections. Periapical lesions developed in all of the eight teeth which were bacterially infected and exposed. Out of ten teeth which were bacterially infected and had cavities without pulp exposure, only two teeth in the acute group demonstrated inflammatory changes and loss of odontoblastic function directly beneath the infected dentinal tubules. Within the limits of the experimental design, this study demonstrated the pulpal responses of the dog with respect to bacteria.
Response of induced periapical lesions in monkeys to a conventional endodontic technique was investigated at varying periods ranging from 15 to 365 days after treatment. The findings indicate that response to treatment is influenced by the extent of the root canal filling, the time lapse between treatment and death, and the presence or absence of bacteria in the apical portion of the canal.
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Paracoccus and Rhodopseudomonas are unusual among bacteria in having a majority of the biochemical features of mitochondria; blue-green algae have many of the features of chloroplasts. The theory of serial endosymbiosis proposes that a primitive eukaryote successively took up bacteria and blue-green algae to yield mitochondria and chloroplasts respectively. Possible characteristics of transitional forms are indicated both by the primitive amoeba, Pelomyxa, which lacks mitochondria but contains a permanent population of endosymbiotic bacteria, and by several anomalous eukaryotic algae, e.g. Cyanophora, which contain cyanelles instead of chloroplasts. Blue-green algae appear to be obvious precursors of red algal chloroplasts but the ancestry of other chloroplasts is less certain, though the epizoic symbiont, Prochloron, may resemble the ancestral green algal chloroplast. We speculate that the chloroplasts of the remaining algae may have been a eukaryotic origin. The evolution or organelles from endosymbiotic precursors would involve their integration with the host cell biochemically, structurally and numerically.
Wallin (1927) first published the notion that the fusion of bacteria with host cells was the principal source of genetic novelty for speciation. He suggested that mitochondria are transitional elements in this process. While the significance that he attributed to symbiosis now seem excessive, he was one of the first authors to be aware of the evolutionary potential of symbiotic events and his view of mitochondria may not seem strange to many cell biologist today. The most significant evolutionary development which has been attributed to intracellular symbiosis is the origin of eukaryotic cellular organization. The current status of the 'serial endosymbiosis hypothesis' is briefly review. The case for the symbiotic origin of the chloroplast, based principally on 16 S RNA oligonucleotide cataloguing, is very strong. Mitochondrial origins are more obscure but also appear to be symbiotic due to recent 18 S cataloguing from wheat embryos. The probablility of the multiple origin of some eukaryotic organelles is also examined, the processes in question being the acquisition of distinct stocks of chloroplasts from disparate photosynthetic prokaryotes and the secondary donation of organelles from degenerate eukaryotic endosymbionts to their hosts, with specific reference to the dinoflagellates Peridinium balticum, Kryptoperidinium foliaceum and the ciliate Mesodinium rubrum. It is concluded that the evolutionary potential of intracellular symbiosis ('cytobiosis': a term introduced in this paper) is great, with the best established influence being on the origin of eukaryotic chloroplasts. Together with the potential effects of viral vectors, symbiosis serves as a supplementary speciation mechanism capable of producing directed evolutionary changes. It is likely that these processes will explain some of the apparent anomalies in evolutionary rates and direction which are not readily explicable by the conventional synthetic theory of evolution.