Evaluation of Nisin F in the Treatment of Subcutaneous Skin Infections, as Monitored by Using a Bioluminescent Strain of Staphylococcus aureus

The potential of nisin F as an antimicrobial agent in treating subcutaneous skin infections was tested in vivo by infecting C57BL/6 mice with a bioluminescent strain of Staphylococcus aureus (Xen 36). Strain Xen 36 has the luxABCDE operon located on a native plasmid. Mice were grouped into four groups: Infected with strain Xen 36 and treated with nisin F, infected with strain Xen 36 and treated with saline (placebo), not infected and treated with nisin (control) and not infected and not treated (control). The immune systems of the mice were suppressed with deksamethasone. Mice were treated with either nisin F or sterile physiological saline 24 and 48 h after infection with subcutaneously injected S. aureus Xen 36 (4 × 10⁶ CFU). Histology and bioluminescent flux measurements revealed no significant difference between infected mice treated with nisin and saline, respectively. However, infected mice treated with nisin F had an increased number of polymorphonuclear cells when compared with infected mice treated with saline. Also, not infected mice treated with nisin F had an influx of polymorphonuclear cells. Nisin F is thus ineffective in combating deep dermal staphylococcal infections. The apparent immune modulation of nisin when subcutaneously injected has to be investigated.     

Bemerkungen über einige Saxifrageen

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VASCULAR INFECTION OF COTTON BY XANTHOMONAS MALVACEARUM (E. F. SMITH) DOWSON

Cotton seedlings raised under glass from seed pre-soaked in a water suspension of Xanthomonas malvacearum , and watered by sub-irrigation only, developed atypical dull green flaccid areas extending from the periphery of the cotyledons. Later symptoms that variably developed were: vascular discoloration, not necessarily continuous, in the petioles of affected cotyledons, in the hypocotyl, and in parts of the plant above the cotyledonary node; premature withering of cotyledons; dull green flaccid areas in true leaves, not necessarily the lowest, later turning brown and drying, with usually a chlorotic margin; parenchymatous attack in stems, petioles and leaves. Evidence is adduced, from the progression of symptoms and from associations between them, and from isolations of the pathogen from various parts of the plant at different stages, that the course of this type of infection is primarily vascular, progressing from the edges of cotyledons into the hypocotyl and thence upwards in vascular tissues. Thence the infection may break out at any time into parenchymatous tissues, leading to the more characteristic forms of the disease, of greater or less severity according to the susceptibility of the parenchyma at the time of its invasion. Similar symptoms have been observed in field plantings, and it is suggested that vascular infection is of greater and wider significance in the epidemiology of bacterial blight than has hitherto been commonly accepted.