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PubMed1994

Anaerobic flora of the conjunctival sac in patients with AIDS and with anophthalmia compared with normal eyes.

Relatively few investigations of anaerobic bacteria as ocular flora have been conducted, and their results have been contradictory. The conjunctival sacs of 22 normal subjects and of 14 patients with acquired immunodeficiency syndrome, and 22 anophthalmic sockets were cultured for anaerobic bacteria Thirty-four (77.3%) of the 44 eyes of normal subjects harbored anaerobic bacteria; Propionibacterium acnes was present in 28 eyes (63.6%), Lactobacillus species in 6 eyes (13.6%), and Veillonella species in 7 eyes (15.9%). The finding were very similar for anophthalmic sockets (p = 0.01), with 17 (77.3%) of the 22 sockets harboring anaerobes; Propionibacterium acnes was the organism identified in 16 (72.7%) of these sockets; Veillonella was identified in 4 (18.1%), Peptococcus niger in 3 (13.6%) and P. granulosum in 2 (9.0%) of these sockets. Acquired immunodeficiency syndrome patients had the highest incidence of anaerobic organisms, with positive cultures obtained from 24 (85.7%) of the 28 eyes. Propionibacterium species were isolated from 16 (57.1%) of these eyes. Clostridium species from 10 (35.7%) eyes and Actinomyces species from 8 (28.6%) eyes. It thus appears that anaerobic organisms are common flora in normal conjunctival sacs and in anophthalmic sockets, as well as in the sacs of acquired immunodeficiency syndrome patients, but the latter group had a higher incidence (x2 = 0.87) and a spectrum of organisms that was different from that of the other two groups.

Acquired Immunodeficiency Syndrome↗
PubMed1979

Eye malformations in rats: induction by prenatal exposure to nickel carbonyl.

Exposure of pregnant rats to inhalation of nickel carbonyl on days 7 or 8 of gestation frequently causes the progeny to develop ocular anomalies, including anophthalmia and microphthalmia. The incidence of extraocular anomalies is very low. The specificity of nickel carbonyl for induction of ocular anomalies in rats appears to be unique among known teratogenic agents.

Abnormalities, Drug-Induced↗
PubMed1990

Genetic ablation in transgenic mice with an attenuated diphtheria toxin A gene.

We have previously generated microphthalmic mice lacking lens fiber cells by targeting the expression of the diphtheria toxin A (DT-A) gene in transgenic mice with regulatory sequences associated with the mouse gamma 2-crystallin gene. Because of the extreme toxicity of DT to animal cells and the potential leakiness of many tissue-specific regulatory regions, we investigated whether there might be an experimental advantage in using a mutant, attenuated form of the DT-A gene (tox-176) fused to gamma 2-crystallin regulatory sequences to ablate fiber cells in the ocular lens. In contrast to the microphthalmia observed in transgenic animals carrying the native DT-A gene, independent lines of mice transgenic for the gamma 2tox176 construct displayed predominantly cataracts or clinical anophthalmia. These contrasting phenotypes were transmitted within each pedigree, although for some lines some phenotypic heterogeneity among offspring was noted. The difference in phenotype between cataractous and clinically anophthalmic transgenic lines could not be ascribed to differences in the transgene copy number. Instead, the results suggest that transgene expression and hence the extent of genetic ablation are modulated by the site of chromosomal integration and, to a lesser extent, by epigenetic events. They also suggest that the attenuated gamma 2tox176 construct can integrate into chromosomal regions that are particularly favorable for expression without compromising embryological development and therefore that the tox-176 gene may be more versatile and effective than the wild-type DT-A gene for achieving genetic ablation with a broad range of cell- or tissue-specific regulatory sequences.

Animals↗
PubMed1998

Geographical variation in anophthalmia and microphthalmia in England, 1988-94.

OBJECTIVE: To investigate the geographical variation and clustering of congenital anophthalmia and microphthalmia in England, in response to media reports of clusters. DESIGN: Comparison of pattern of residence at birth of cases of anophthalmia and microphthalmia in England in 1988-94, notified to a special register, with pattern of residence of all births. Three groups studied included all cases, all severe cases, and all severe cases of unknown aetiology. OUTCOME MEASURES: Prevalence rates of anophthalmia and microphthalmia by region and district, and by ward population density and socioeconomic deprivation index of enumeration district grouped into fifths. Clustering expressed as the tendency for the three nearest neighbours of a case to be more likely to be cases than expected by chance, or for there to be more cases within circles of fixed radius of a case than expected by chance. RESULTS: The overall prevalence of anophthalmia and microphthalmia was 1.0 per 10 000 births. Regional and district variation in prevalence did not reach statistical significance. Prevalence was higher in rural than urban areas: the relative risk in the group of wards of lowest population density compared with the most densely populated group was 1.79 (95% confidence interval 1.15 to 2.81) for all cases and 2.37 (1.38 to 4. 08) for severe cases. There was no evidence of a trend in risk with socioeconomic deprivation. There was very little evidence of localised clustering. CONCLUSIONS: There is very little evidence to support the presence of strongly localised environmental exposures causing clusters of children to be born with anophthalmia or microphthalmia. The excess risk in rural areas requires further investigation.

Anophthalmos↗