Onset of penicillin-induced bacteriolysis in staphylococci is cell cycle dependent.

Synchronously growing staphylococci were treated with "lytic" concentrations of penicillin at different stages of their division cycle. Coulter Counter measurements and light microscopy were used to determine the onset of bacteriolysis. Independent of the stage of the division cycle at which penicillin was added, (i) the cells were always able to perform the next cell division; (ii) the following division, however, did not take place; and (iii) instead, at this time, when the onset of the subsequent cell separation was observed in control cultures, lysis of the penicillin-treated cells occurred. These results support a recent model (P. Giesbrecht, H. Labischinski, and J. Wecke, Arch. Microbiol. 141:315-324, 1985) explaining penicillin-induced bacteriolysis of staphylococci as the result of a special morphogenetic mistake during cross wall formation.     

High state of order of isolated bacterial lipopolysaccharide and its possible contribution to the permeation barrier property of the outer membrane.

The conformational properties of the isolated S form of Salmonella sp. lipopolysaccharide (LPS), of Re mutant LPS, and of free lipid A were investigated by using X-ray diffraction and conformational energy calculations. The data obtained showed that LPS in a dried, in a hydrated, and probably also in an aqueous dispersion state is capable of forming bilayered lamellar arrangements similar to phospholipids. From the bilayer packing periodicities, a geometrical model of the extensions of the LPS regions lipid A, 2-keto-3-deoxyoctulosonic acid, and O-specific chain along the membrane normal could be calculated. Furthermore, the lipid A component was found to assume a remarkably high ordered conformation: its fatty acid chains were tightly packed in a dense hexagonal lattice with a center-to-center distance of 0.49 nm. The hydrophilic backbone of lipid A showed a strong tendency to form domains in the membrane, resulting in a more or less parallel arrangement of lipid A units. According to model calculations, the hydrophilic backbone of lipid A appears to be oriented approximately 45 degrees to the membrane surface, which would lead to a shed roof-like appearance of the surface structure in the indentations of which the 2-keto-3-deoxyoctulosonic acid moiety would fit. In contrast, the O-specific chains assume a low ordered, heavily coiled conformation. Comparison of these structural properties with those known for natural phospholipids in biological membranes indicates that the high state of order of the lipid A portion of LPS might be an important factor in the structural role and permeation barrier functions of LPS in the outer membrane of gram-negative bacteria.     

Neither an enhancement of autolytic wall degradation nor an inhibition of the incorporation of cell wall material are pre-requisites for penicillin-induced bacteriolysis in staphylococci

In contrast to what has been postulated, penicillin G at its optimal lytic concentration of 0.1 g per ml did not lead to a detectable activation of autolytic wall processes in staphylococci in terms of the release of uniformly labelled wall fragments from cells pretreated with the drug for 1 h. Rather a considerable inhibition of this release was observed. A similarly profound inhibition of the release of peptidoglycan fragments occurred when staphylococci pretreated for 1 h with 0.1 g penicillin per ml acted as a source of crude autolysins on peptidoglycan isolated from labelled normal cells of the same strain. This clearly demonstrated that the overall inhibition of autolytic wall processes caused by penicillin was mainly due to a decreased total autolysin action rather than to an altered wall structure. Furthermore, no substantial penicillin-induced inhibition of the incorporation of ¹⁴C-N-acetylglucosamine into the staphylococcal wall could be observed before bacteriolysis started, i. e., approximately during the first 80 min of penicillin action. These results are not consistent with any of the models hitherto proposed for the action of penicillin.Dedicated to Prof. Dr. Gerhart Drews on the occasion of his 60th birthday     

Rhodopseudomonas viridis,nov. spec., ein neu isoliertes,obligat phototrophes Bakterium

Zusammenfassung Nach Untersuchung von Morphologie, Feinstruktur und Ernährungsphysiologie wird ein neu isoliertes grünes Bakterium in die Gattung Rhodopseudomonas eingeordnet und der Artname Rhodopseudomonas viridis vorgeschlagen.

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Summary Rhodopseudomonas viridis was isolated from different waters near Freiburg im Breisgau. It is a gramnegative bacterium which is motile by means of polar flagella. Cells are usually distinctly rod-shaped, occasionally the rods are lightly curved. The size is variable, the dimensions 0.6 to 0.8 by 1.5–2.5 . Dense suspensions of this Rhodopseudomonas species are green coloured. The colour is changed in older cultures to a dirty brown-green. The absorption-maxima of the in-vivo spectrum at 400, 606 and 1020 nm are attributed to bacteriochlorophyll b, while the peaks at 451 and 483 nm reflect the presence of carotenoids. The bacteria grow only anaerobically in the light. They are strictly photo-organotroph. Heavy growth is observed in media which contain malate, succinate, pyruvate or acetate as carbon source and ammonia as nitrogen source. p-amino-benzoic acid, biotin and vitamin B are required. Yeast extract (0.05%) and casamino acids stimulate but fatty acids with the exception of acetate inhibit growth. No development is observed with carbon dioxide as sole carbon source. Gelatine is not liquefied. Nitrate is not reduced to nitrite.

     

A novel, “hidden” penicillin-induced death of staphylococci at high drug concentration,occurring earlier than murosome-mediated killing processes

In log-phase cells of staphylococci, cultivated under high, non-lytic concentrations of penicillin G, there occurred a novel killing process hitherto hidden behind seemingly bacteriostatic effects. Two events are essential for the apprearance of this hidden death: (i) the failure of the dividing cell to deposit enough fibrillar cross-wall material to be welded together, and (ii) a premature ripping up of incomplete cross walls along their splitting system. Hidden death started as early as 10–15 min after drug addition, already during the first division cycle. It was the consequence of a loss of cytoplasmic constituents which erupted through peripheral slit-like openings in the incomplete cross walls. The loss resulted either in more or less empty cells or in cell shrinkage. These destructions could be prevented by raising the external osmotic pressure. In contrast, the conventional non-hidden death occurred only much later and exclusively during the second division cycle and mainly in those dividing cells, whose nascent cross walls of the first division plane had been welded together. These welding processes at nascent cross walls, resulting in tough connecting bridges between presumptive individual cells, were considered as a morphogenetic tool which protects the cells, so that they can resist the otherwise fatal penicillin-induced damages for at least an additional generation time (morphogenetic resistance system). Such welded cells, in the virtual absence of underlying cross-wall material, lost cytoplasm and were killed via ejection through pore-like wall openings or via explosions in the second division plane and after liberation of their murosomes, as it was the case in the presence of low, lytic concentrations of penicillin. Bacteriolysis did not cause any of the hitherto known penicillin-induced killing processes.Dedicated to Prof. Dr. Georg Henneberg on the occasion of his 85th birthday     

Bicyclo[3,2,1]octanoid,neolignans from Aniba simulans

Six bicyclo[3,2,1]octanoid neolignans, isolated from the benzene extract of Aniba simulans Allen (Lauraceae) trunk wood, are shown to derive from two basic structures: 1-allyl-8-hydroxy-6-(3′-methoxy-4′,5′-methylenedioxyphenyl)-7-methyl-3-oxobicyclo[3,2,1]octane, substituted by 4-hydroxy, 4-hydroxy-5-methoxy, 4-methoxy or 4,5-dimethoxy groups; and 1-allyl-8-hydroxy-6-(3′-methoxy-4′,5′-methylenedioxyphenyl)-7-methyl-4-oxobicyclo[3,2,1]oct-2-ene, substituted by 3-hydroxy or 3-hydroxy-5-methoxy groups. The structural proposals are based on spectral data, interconversions synthesis of a derivative from the known (2R,3S,3aS)-3a-allyl-5-methoxy-2-(3′-methoxy,4′,5′-methylenedioxyphenyl)-3-methyl-2,3,3a,6-tetrahydro-6-oxobenzofuran.     

Mechanism of detection of resistive loads in conscious humans.

Conscious humans easily detect loads applied to the respiratory system. Resistive loads as small as 0.5 cmH2O.l-1.s can be detected. Previous work suggested that afferent information from the chest wall served as the primary source of information for load detection, but the evidence for this was not convincing, and we recently reported that the chest wall was a relatively poor detector for applied elastic loads. Using the same setup of a loading device and body cast, we sought resistive load detection thresholds under three conditions: 1) loading of the total respiratory system, 2) loading such that the chest wall was protected from the load but airway and intrathoracic pressures experienced negative pressure in proportion to inspiratory flow, and 3) loading of the chest wall alone with no alteration of airway or intrathoracic pressure. The threshold for detection for the three types of load application in seven normal subjects was 1.17 +/- 0.33, 1.68 +/- 0.45, and 6.3 +/- 1.38 (SE) cmH2O.l-1.s for total respiratory system, chest wall protected, and chest wall alone, respectively. We conclude that the active chest wall is a less potent source of information for detection of applied resistive loads than structures affected by negative airway and intrathoracic pressure, a finding similar to that previously reported for elastic load detection.     

1,3-diaryl-propanes and propan-2-ols from Virola species

The trunk woods of two Amazonian Myristicaceae, Virola minutiflora and V. elongata, contain respectively 1-(2-hydroxy-4-methoxyphenyl)-3-(3,4-m     

Die Bezeichnung des Stammes F von Rhodopseudomonas viridis als Typ-Stamm

Ohne Zusammenfassung