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Biomedical subjects

G N Dutton

Publications and source records attributed to G N Dutton.

At least 127 records · Page 7Linked to original sources
PubMed1986

Clinicopathological features of a congenital murine model of ocular toxoplasmosis.

Sequential clinical examination was carried out upon the eyes of mice that had been infected in utero with Toxoplasma gondii. Three patterns of clinical disease were seen. First, crystalliform cataracts, which either remained unchanged in character or occasionally became more extensive, were observed. Second, acute uveitis occurred in a small proportion of eyes, progressing into a chronic inflammatory disease with secondary opaque cataract. The third pattern comprised multiple discrete foci of deep retinal disturbance. It is suggested that these lesions were attributable to focal macrophage clusters in the sub-retinal space with overlying dome-shaped elevations of the photoreceptor matrix. The severity of disease, as assessed clinically, correlated with the underlying histopathology but not with the serological titres against Toxoplasma. Immunocytochemical staining for Toxoplasma antigen revealed only intra-retinal Toxoplasma cysts, but no free organisms or extracystic antigen were demonstrated. Selective photoreceptor destruction was the most prominent histopathological feature, implicating auto-immune mechanisms of tissue destruction.

Acute Disease↗
PubMed1986

The ultrastructural pathology of congenital murine toxoplasmic retinochoroiditis. Part I: The localization and morphology of Toxoplasma cysts in the retina.

This study describes the ultrastructural characteristics of retinal parasitization by Toxoplasma gondii in a congenital mouse model. Forty-two eyes from infected mice, 18-22-weeks-old, and 24 control eyes were initially studied by light microscopy of semithin sections. Twenty-six eyes from infected animals and six from the controls were further investigated by transmission electron microscopy. A total of 13 Toxoplasma cysts was found in samples of the retinas of six eyes from five infected animals. These were located in the inner retina, particularly the ganglion-cell layer, but in no other ocular tissue. The cyst wall interdigitated with the host cell which in most cases was probably glial in origin (Müller cell). Two cysts showed evidence of parasitization of neural cells. The individual Toxoplasma cystozoites demonstrated characteristic ultrastructural features. There was no evidence of morphological changes indicative of toxicity to surrounding retinal tissues, and the associated inflammatory cell reaction (described in Dutton, McMenamin, Hay and Cameron, 1986b) was remote from the parasite. There was no morphological evidence of rupture or degeneration of cysts. No free parasites (endozoites) or pseudocysts were observed.

Animals↗
PubMed1986

The ultrastructural pathology of congenital murine toxoplasmic retinochoroiditis. Part II: The morphology of the inflammatory changes.

A congenital murine model of toxoplasmic retinochoroiditis was employed to study the ultrastructural pathology of retinal parasitization by Toxoplasma gondii. Forty-two eyes from infected mice (18-22-weeks-old) and 24 eyes from control animals were studied by light microscopy (semithin sections). Twenty-six of the eyes from infected animals and six from the control group were subsequently selected for transmission electron microscopy. Control tissues showed no significant abnormality. The pathological changes in diseased tissues ranged in severity from low-grade mononuclear cell infiltration in the subretinal space to complete destruction of the outer retina, the retinal pigment epithelium and the choroid in the presence of a granulomatous inflammatory reaction. Phagocytosis of photoreceptor outer segments by macrophages was observed. Both macrophages and lymphocytes appeared to mediate photoreceptor lysis in eyes which were moderately affected by the disease. Severely affected eyes exhibited vasculitis and inflammatory cell invasion into the vitreous. A lymphoplasmacytoid cell infiltrate was present in the outer retina and choroid in these eyes. There was no evidence that Toxoplasma cysts provided foci for inflammatory cell attack.

Animals↗
PubMed1986

Neodymium-YAG laser in the management of posterior capsular opacification--complications and current trends.

Opacification of the posterior capsule of the lens frequently complicates extra capsular cataract surgery. The recent development of the pulsed YAG laser for the division of structures in the anterior segment of the eye has provided a novel means of restoring visual acuity following this complication. The complications of this procedure are described and discussed in the light of a preliminary study aimed at investigating changes taking place within the anterior chamber of the eye during the 24 hour period following application of laser treatment. No major problems were noted in 10 patients undergoing Q-switched Neodymium-YAG laser capsulotomy. The intra-ocular pressure was transiently raised following this procedure in 4 patients. In each case this decreased spontaneously. No changes in anterior chamber depth or gonioscopic appearances were observed. The current trends in the preferred technique for cataract surgery were assessed for the Western District of Glasgow. Extra-capsular surgery comprised 18.7 per cent of the total number of operations in 1980 and 1981; this increased to 55.5 per cent by 1984 to 1985 with a concomitant increase in the number of posterior capsulotomies performed. The implications of these results in terms of future health care planning are discussed.

Cataract Extraction↗
PubMed1986

The causes of tissue damage in toxoplasmic retinochoroiditis.

The pathogenetic mechanisms of tissue damage in toxoplasmic retinochoroiditis are complex and incompletely understood. They include invasion and parasitisation of retinal tissues by the Toxoplasma parasite and localised tissue damage by a complex associated immune response. Clinical and experimental studies which shed light upon our understanding of the disease process are reviewed and discussed with regard to current policies in treatment.

Animals↗
PubMed1985

Congenital toxoplasmic retinochoroiditis in the mouse--the use of the peroxidase anti-peroxidase method to demonstrate Toxoplasma antigen.

The peroxidase anti-peroxidase immunocytochemical staining method has been used to demonstrate Toxoplasma antigen within paraffin-embedded sections of the eyes of mice congenitally infected with Toxoplasma. Intact Toxoplasma tissue cysts were demonstrated within the retina but in no other ocular structure. No endozoites and no extra-cystic antigens were detected by this technique within any of the eyes examined. The possible implications of these findings in relation to the pathogenesis of toxoplasmic retinochoroiditis are discussed.

Animals↗
PubMed1985

Candidal endophthalmitis in Glaswegian heroin addicts: report of an epidemic.

Nine heroin addicts with presumed candidal endophthalmitis were seen in Glasgow between November 1982 and April 1984. Six patients during a two month period in 1983. The physical symptoms and signs observed, results of laboratory investigations and responses to anti-fungal chemotherapy are reported. Epidemiological factors relating to possible sources of infection are explored.

Adolescent↗
PubMed1984

Congenital toxoplasmic retinochoroiditis in a mouse model.

A study of the eyes of adult mice infected in utero with Toxoplasma gondii is reported. The histopathological features of the ocular inflammatory response in the infected mice ranged from minimal damage to complete destruction of the retinal tissue. Notable features such as retinal vasculitis and an almost uniform and highly selective destruction of the photoreceptor layer of the retina suggest a similarity between experimental autoimmune retinitis and the disease process in the retinas of our Toxoplasma-infected mice. We suggest that our mouse model could provide a simple and inexpensive tool for the investigation of immuno-pathological processes in the retina resulting from congenital Toxoplasma infection. The model has the advantage of low post-natal mortality coupled with high ocular morbidity. Furthermore, its aetiology is probably analogous to that of human ocular toxoplasmosis, in that the foetus becomes infected in utero via a mother whose primary infection is acquired during gestation.

Animals↗
PubMed1983

A murine model of congenital toxoplasmic retinochoroiditis.

A histopathological study of toxoplasmic retinochoroiditis in 39 eyes of mice infected in utero with Toxoplasma gondii and sacrificed at 16 weeks post-partum showed a wide variation in the pattern of tissue destruction. The changes in individual eyes were graded from mild to severe; Toxoplasma cysts were present in the retina and optic nerve in each grade. In the least affected eyes, Toxoplasma cysts were rarely seen and the disease was limited to a low grade uveitis and retinal lymphocytic perivasculitis. In the more severely affected eyes, there was focal, sectorial or total retinal destruction with secondary degeneration in the lens. In some eyes inflammatory destruction of the outer retina was associated either with a paucity of cells, or with lymphocytic infiltration or with plasma cell infiltration; giant cell granulomatous reactions were rare. In the most severely affected eyes the retina was necrotic and calcified. The findings illustrate the complexity of toxoplasmic retinochoroiditis and suggest that autoimmunity may play a part in the disease process.

Animals↗
PubMed1983

Toxoplasmic retinochoroiditis--current concepts in pathogenesis.

The pathogenesis of retinochoroidal destruction associated with infection by Toxoplasma gondii presents a perplexing problem. A murine model of congenital toxoplasmic retinochoroiditis is described in relation to the current concepts regarding the pathogenesis of the disease process in man. It would appear that in this model at least, auto-immune mechanisms may contribute to the inflammatory process.

Animals↗
PubMed1982

Pupillary fatigue in myasthenia gravis.

By shining a narrow beam of light upon the pupillary margin, a sustained oscillation of pupil size or hippus, may be induced; the frequency of which is dependent upon the rate of conduction along the neuronal pathways subserving pupillary function. This manoeuvre has been carried out upon a series of twelve patients with myasthenia gravis, eleven of whom demonstrated a gradual diminution in oscillation frequency. This is compared with twelve control subjects, only one of whom demonstrated a significant decline in oscillation rate. The mean gradients were 0.0 +/- 0.4 cycles/min for the control subjects and -2.4 +/- 0.4 cycles/min for the patients with myasthenia. These gradients differ significantly p less than 0.0001. It is suggested that the pupillary reaction to light may be fatigued by exercising it at its maximum intrinsic rate in patients with myasthenia gravis.

Adult↗
PubMedDate not supplied

Measurement of ascorbic acid in human aqueous humour and plasma and bovine aqueous humour by high-performance liquid chromatography with electrochemical detection.

High-performance liquid chromatography (HPLC) on ODS silica with cetyltrimethylammonium bromide as an ion-pairing reagent and electrochemical detection (ECD) was used to determine ascorbic acid in bovine and human aqueous humour and human plasma. Hydroquinone was used as the internal standard. A calibration curve plotted with ascorbic acid concentrations in the range 0.5-5 micrograms ml-1 for peak height versus internal standard peak height had a correlation coefficient of 0.998. The RSD (precision) between analyses of the same diluted sample was 1.5% and the RSD (reproducibility) between analyses of separate aliquots of the same sample of aqueous humour was 1.6%.

Animals↗
PubMedDate not supplied

Congenital corneal anesthesia.

Congenital corneal anesthesia is a rare clinical entity that poses a diagnostic dilemma, particularly in the pediatric age group. The sensory deficit may be confined to the cornea, or extend to other divisions of the trigeminal nerve. The sensory deficit may occur as an isolated abnormality, as part of a complex neurological syndrome, or it may occur in association with multiple somatic abnormalities and congenital insensitivity to pain. This condition usually presents between the ages of 8 to 12 months. Poor vision, photophobia, conjunctival injection, and corneal ulceration in the absence of pain and distress in a child should alert the clinician to the possibility of anesthetic cornea. In the early stages of presentation, punctuate keratopathy is the main feature, which may progress to non-healing persistent corneal epithelial defects. This stage may progress to acute corneal lysis and perforation. In most patients, conservative approaches such as copious lubrication, prevention of self-harm and cautious use of bandage contact lenses are effective in preventing progressive corneal damage. Tarsorrhapy is effective in promoting epithelial healing and permanent lateral tarsorraphy may prevent further development of epithelial defects. Amniotic membrane graft may be considered in order to improve epithelial healing. Corneal grafts carry a poor prognosis. Accurate initial diagnosis, evaluation, and proper management are paramount to prevent visual loss due to long-term complications of corneal anesthesia. This review of the literature outlines the problems and approaches in diagnosis, evaluation, and management of this rare condition.

Cornea↗