Plasma Temperature in Optical Field Ionization of Gases by Intense Ultrashort Pulses of Ultraviolet Radiation.
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Biomedical subjects
Publications and source records attributed to W Blyth.
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This paper reports the microbiological aspects of zosteriform spread of herpes simplex virus (HSV) to the eye in the NIH strain of inbred mouse. Microbiological data support the concept of true zosteriform spread of herpes simplex virus from the inoculation site on the snout to the trigeminal ganglion, and thence to the eye. Following zosteriform spread of HSV to the eye, there is a frequent bacterial superinfection and this is associated with a typical clinical picture. Treatment of the mice with intensive systemic and topical antibiotics is able to alter the frequency with which this type of keratitis is seen.
When herpes simplex virus (HSV) is inoculated onto the snout of the inbred strain NIH mouse, clinical disease of the eye ensues only after a delay, due to spread of virus to the eye occurring via neural pathways. This report is concerned with the detailed description of eye disease. Physical signs observed include mydriasis, iritis and keratitis. The incidence of combinations of physical signs has been analysed by the computer and presented as pie-charts to show the complexity and evolution of the eye disease.
A murine model of zosteriform spread of herpes simplex virus to the eye is reported. Viral antigens were demonstrated by a peroxidase-antiperoxidase technique in the trigeminal ganglion, iris, ciliary body, and cornea. The histology suggested a spontaneous bacterial superinfection during the later stages of the herpetic disease of the cornea. The relevance to human disease is discussed.
Spore walls of a sputum-derived isolate of Aspergillus clavatus yielded mutagen(s) when their extracts were fractionally precipitated with ethanol following alkaline hydrolysis. After spores were given by nasal inoculation to 6-8-week-old CF-1 mice, light and electron microscopy of lung sections showed that they had been readily phagocytozed by the polymorphonuclear leucocytes and alveolar macrophages mobilized during early allergic alveolitis in immunized mice. The formation of phagosomes was followed in thioglycollate-stimulated peritoneal macrophages grown in vitro. Unimmunised mice showed a comparable lung reaction, attributed to pulmonary mycotoxicosis, and revealed a rising incidence of lung tumours, from 25% at 2 months from inoculation, to 27.3% at 6 and to 55.5% at 8. Mean numbers of tumours per lung rose from 1.0 to 2.2. Total tumours, including lymphomas, reached a final incidence of 77.7% at 8 months, when control animals were tumour-free. Tumour development correlated with the retention of apparently intact spores within giant cells probably derived from aggregates of alveolar macrophages. The implications of these findings in the light of the known history of human exposure to such spores is discussed.
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Prednisolone potentiated candidiasis in mice when given as dosages of 1 mg, s.c. at-1 and + 24 h in relation to the time of inoculation, i.p. with any of 4 isolates of C. albicans which differed in degree of pathogenicity. Enhancement was shown by increased intra-abdominal colonisation, haematogenous dissemination and percentage mortality. There was at least a seven-fold increase in the mean area occupied by fungal colonies in median, longitudinal sections of kidneys after prednisolone treatment. Compared with those of fungal controls, renal lesions were deficient in inflammatory cells, only a few polymorphonuclear leukocytes occurring peripherally. Amphotericin B (AmB) at a non-toxic, total dosage of 0.5 mg given in two injections of 0.25 mg, i.p. at intervals of 24 h rendered infections non-lethal, or significantly reduced their severity, when started 24 or 48 h after inoculation. When antifungal treatment was delayed until 72 h, however, early deaths occurred despite the fact that the mean renal section area occupied by pseudomycelium was little more than that of controls and fibrosis of lesions was characteristic. Early mortalities increased even further when AmB, commencing at 72 h, was combined with prednisolone. This effect was thought to be due to the release of some toxic factor(s) following the leaching of cells by AmB combined with depleted antibody levels. Ascitic fluids from infected mice given Ehrlich ascites tumour cells showed marked increases in the concentrations of alpha2 and gamma globulins. Concentrations were almost reduced to normal levels in animals treated with prednisolone and/or AmB.
The principal ultrastructural changes in cells of Candida albicans treated with amphotericin B (AmB), either in vitro or in vivo, and in the presence or absence of prednisolone included plasmolysis, vacuolation and destruction of organelles. Lamination of the cell wall, although discernible after 4 h antibiotic treatment in vitro, was conspicuous in vivo, especially in prednisolone-treated mice given AmB 72 h after inoculation and was seen in both phagocytosed cells and those free in inflammatory exudates. Somatic extracts from control cells and somatic extracts and leachates from AmB-treated cells showed the presence of low-grade toxic components when given i.p. to mice receiving antinomycin D(AMD) s.c. Culture filtrates were negative. Eighteen hour cultures were more toxic than those grown for 3 days and no toxicity was shown for cultures after 8 or 14 days. The behaviour of toxic materials during electrophoresis in polyacrylamide gels suggested that they were proteins of relatively high molecular weight.
Five groups of antigens were identified in culture filtrates and extracts from spores and mycelia of Aspergillus clavatus fractionated by gel filtration, affinity chromatography, electrophoresis in polyacrylamide gels and chemical analysis. Some particulate and soluble fractions given by nasal inoculation provoked murine allergic alveolitis in non-sensitized and sensitized precipitin-negative, and sensitized, precipitin-positive, animals. Alveolitis-inducing substances appeared to be glycoprotein precipitinogens, which withstood proteolysis, were preferentially adsorbed by concanavalin A, but which were rendered almost inert by sodium periodate oxidation. Spore walls were particularly rich in allergenic substances extractable by alkaline hydrolysis. Delipidated dead spores provoked more severe disease in all immunological groups of mice than live spores. Polysacchraride extracts and acid hydrolysates of spore walls were unreactive.
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Mycological and serological studies were carried out as part of a survey of respiratory disease in Scottish maltworkers. 70% of stained sputum smears from 574 workers showed the presence of higher plant cells and/or myclelia, and the spores of common environmental fungi. Penicillium spp. (90%), Rhizopus stolonifer (48%) and yeasts (53%) were the dominant fungi in 699 sputum cultures, and showed a similar proportional distribution in 327 samples of grain, malt, culms and dusts from fifty-six maltings. 57% of 711 men were serologically positive for fungi, 22% for Aspergillus fumigatus, 20% for A. clavatus, 10% for A. niger, 16% for Cladosporium herbarum and over 3% for Rhizopus stolonifer, 6% of 132 men were positive for Penicillium cyclopium. No precipitating antibodies to antigens from Alternaria tenuis, Aureobasidium pullulans, Candida albicans, Geotrichum candidum, Rhodotorula glutinis or Trichoderma viride were detected in tests of forty sera. Sera from the 5.2% of men with symptoms of extrinsic allergic alveolitis showed increased reactivity to mycelial antigens from Aspergillus clavatus. The fungus was cultured from 21% of maltings, 7% of all environmental samples and from the sputa of 8% of maltworkers.
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In a survey of respiratory disease in the Scottish malting industry 5.2% of employees were found to have symptoms of extrinsic allergic alveolitis. In most cases the disease was mild and not associated with any serious respiratory disability. It was significantly less common where modern mechanical methods of malting were used. Mycological and serological studies suggested that it was usually caused by a type 3 allergic reaction to Aspergillus clavatus.
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In a survey of the farming population of Orkney, Ayrshire, and East Lothian the prevalence of farmer's lung was estimated at 86 per 1,000 in both Orkney and Ayrshire and 23 per 1,000 in East Lothian. If cases with a negative farmer's lung hay (F.L.H.) precipitin test are excluded these figures are reduced to 43, 36, and nil respectively, but those for Orkney and Ayrshire are still about 20 times higher than any figure previously reported for the prevalence of farmer's lung in Britain.Regional variations in prevalence are probably related both to climatic conditions and to differences in agricultural methods, the latter often being dictated by economic circumstances. Nevertheless the prevalence of farmer's lung could be reduced considerably by the energetic application of preventive measures, backed by financial incentives. The most important of these are efficient drying of hay and cereals before storage, more extensive use of silage, better ventilation of farm buildings, and the introduction of mechanical feeding systems. Individual farmworkers could be taught how to recognize the early symptoms of the disease and encouraged to wear respirators when handling mouldy fodder.
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