Oriented Adhesion of Escherichia coli to Polystyrene Particles

ABSTRACT The adhesion of nonflagellated Escherichia coli strain K-12 to polystyrene (PS) latex spheres or glass capillaries has been observed by using several techniques. Attention was focused on the orientation of the rod-shaped bacteria as they adhered to the surfaces in 100 mM phosphate-buffered saline. Data show that PS particles adhered to the ends of the bacteria more than 90% of the time. Moreover, the PS particles adhered to one end only, never to both. Similarly, for experiments with bacteria adhering to glass, the bacteria adhered on their ends. In order to determine whether the end of a bacterium had a different charge density from that of the middle, rotational electrophoresis experiments were used. These experiments indicated no measurable charge nonuniformity. In order to examine how strongly adhered the bacteria were to the PS particles, differential electrophoresis was used. Almost always, bacteria were found to be irreversibly adhered to the PS spheres. The cause of the oriented adhesion is not likely due to surface lipopolysaccharides (LPS), since the three strains of K-12 that were used, each having a different length of LPS, showed similar behavior. The results are discussed in terms of bacterial cell polarity. The data indicate that nanodomains on the bacterial ends are important for adhesion and that the time scale for irreversible adhesion is short.

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Decreased sensitivity to polymyxin B in colicin K tolerant cells of Escherichia coli K-12 in the presence of colicin K

Canadian Journal of Microbiology ◽

10.1139/m73-057 ◽

1973 ◽

Vol 19 (3) ◽

pp. 345-351 ◽

Cited By ~ 1

Author(s):

L. G. Mathieu ◽

D. Legault-Hetu

Keyword(s):

Escherichia Coli ◽

Cell Wall ◽

Bacterial Cell ◽

Morphological Changes ◽

Wild Strain ◽

Lethal Effect ◽

Polymyxin B ◽

Bacterial Cell Wall ◽

Receptor Sites ◽

K 12

Cells refractory to the lethal effect of colicin K were selected from a sensitive Escherichia coli K-12 strain. They could still be lysed by bacteriophage T6 which is thought to share with colicin K common receptor sites on the bacterial cell wall. Incubation of these cells for 30 min in a colicin K preparation considerably reduced its subsequent activity on the sensitive parent strain. When these tolerant cells were exposed to polymyxin B in the presence of colicin K, the lethal activity of the polymyxin was decreased significantly as compared with that exerted by the antibiotic in the absence of colicin K. In the colicin K sensitive wild strain, the combined lethal effect of the bacteriocin and of the antibiotic was not smaller than that of either inhibitor alone. Examination with the fluorescence microscope of cells stained with acridine orange showed that colicin K tolerant cells incubated with polymyxin B had undergone greater morphological changes than similar cells treated with polymyxin B in the presence of colicin K. Leakage of materials absorbing at 260 nm was greatest for the cells exposed to polymyxin B alone. The results suggest that in colicin K tolerant cells of E. coli derived from a sensitive strain, the bacteriocin might compete with polymyxin B for sites of attachment on the bacterial cell wall or mask some of the envelope phospholipids which are believed to react with polymyxin B.

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