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To report a case of archipelago keratitis and its improvement as evaluated by corneal densitometry. JavaScript is currently disabled, this site works much better if you enable JavaScript in your browser.
Top of pageAbstractThe classification system of congenital corneal opacification (CCO) may be better considered from a perspective of pathogenesis, surgical intervention, and prognosis. Traditional need not mean old in this context, because even very recent articles1 concerning this subject have perpetuated a classification system which does not lend itself to application for useful assessment of surgical or management outcomes.
A 57-year-old man presented with blurred vision associated with photophobia and halos around lights. Formation of the anterior chamber and therefore by implication, the cornea, is a complex developmental process that involves the lens, head ectoderm, neuroectoderm, primitive mesoderm, and neural crest cells. Secondary CCO may be best considered as cases of kerato-irido-lenticular dysgenesis (KILD) and other secondary causes including infection, iatrogenic, developmental anomalies of the iridotrabecular system or lens or both, and developmental anomalies of the adnexal. As will unfold in this article, terminology is crucial to furthering our understanding of this complex subject.Describing a developmental corneal opacity as being Peters' anomaly is akin to diagnosing someone with a respiratory problem as having a cough. It is neither precise, diagnostic, nor informative about prognosis.Peters2 described a condition affecting the cornea approximately 100 years ago when high-frequency ultrasound (HFU) and ocular coherence tomography (anterior segment) were not available. The treatment was changed to topical steroids and oral acyclovir and a diagnosis of archipelago keratitis was made. Terminology is crucial to furthering our understanding of the formation of the anterior chamber if we are to do so by studying cases of CCO.
Clinicopathological correlation of congenital corneal opacification using ultrasound biomicroscopy. The patient showed quick response to the treatment and the infiltrates disappeared within 5 weeks.
Both can coexist with glaucoma.4, 5 CHED always occurs at birth, whereas PPMD may occur at birth (Figure 1). This classification of primary and secondary CCO with its subclassifications cannot be made by clinical examination alone and necessitates other diagnostic assessments.
Type 1 CHED (CHED I) tends to be autosomal dominant and less severe, whereas type 2 tends to be autosomal recessive and more severe6 (Figure 2). A clinicopathologic study of posterior polymorphous dystrophy:implications for pathogenetic mechanism of the associated glaucoma. We describe the use of corneal densitometry complementary to slit-lamp examination in the clinical observation of archipelago keratitis. The suggestion then is that primary congenital glaucoma is also a neurocristopathy,9 again resulting due to a sheet of primordial endothelium failing to fenestrate appropriately within the angle and causing the iris to insert high and flat (Figure 3).
Posterior polymorphous corneal dystrophy in Czech families maps to chromosome 20 and excludes the VSX1 gene. This tissue almost causes the iris root to 'hang up', with goniotomy allowing release of the iris root and exposing trabecular meshwork. Autosomal recessive corneal endothelial dystrophy (CHED2) is associated with mutations in SLC4A11. Iris root (white arrow), ciliary body band (dotted white arrow), trabecular meshwork (dashed white arrow).

There is an amorphous type material obscuring the trabecular meshwork partially (white star).
Some authors prefer to term this sclerocornea plana but this author feels this is confusing. In isolated sclerocornea (Figure 4), the anterior chamber is visible and the eye is not microphthalmic. Congenital familial cornea plana with ptosis, peripheral sclerocornea and conjunctival xerosis. This is a primary CCO as the lens and iris are normal.Full figure and legend (83K)In complex sclerocornea, there may be associated microphthalmos, cataract, infantile glaucoma, or any combination of these16 (Figure 5). There is usually always a relative central clearing but the thickness of this relatively clear area is normal or increased, never reduced (see Figure 6). A forkhead gene, FoxE3, is essential for lens epithelial proliferation and closure of the lens vesicle. Traditionally this would be classed as sclerocornea but the disruption of the anterior segment warrants another classification. Keratolenticular dysgenesis is proposed whereby the lens vesicle separates but then fails to form appropriately.
Abnormal eye development associated with Cat4a, a dominant mouse cataract mutation on chromosome 8. However, there is clearly anterior displacement of the limbus as might be seen in sclerocornea. This displacement is asymmetric and peritomy reveals the true extent of the corneal tissue.
Keratolenticular dysgenesis (Peters' anomaly) as a result of acute embryonic insult during gastrulation.
Additionally lack of a proliferating anterior lens epithelium leads to absence of secondary lens fibres and a dysplastic, cataractous lens. For example, see Figure 9 showing disruption of the lens with kerato-irido-lenticular dysgenesis (KILD). On the basis of HFU and clinical appearance it is much more likely that the case in Figure 9 would have a FOXE3 mutation rather than the case in Figure 10. On the left there is vascularization of the cornea with opacification which corresponds to the area of posterior corneal defect and iridocorneal adhesion with abnormal iris stroma (white arrows) on the HFU.
On the right side there is clear keratolenticular dysgenesis with disruption of the lens (white arrow) and anterior capsule (dashed arrow) and a posterior corneal defect (black arrow). Changes in corneal ultrastructure resulting from early lens removal in the developing chick embryo. A novel homeobox gene PITX3 is mutated in families with autosomal-dominant cataracts and ASMD. Deletion in the promoter region and altered expression of Pitx3 homeobox gene in aphakia mice. The vascularization seen in the clinical picture is within the iris and likely due to persistent pupillary membranes and not the cornea. Homozygous nonsense mutation in the FOXE3 gene as a cause of congenital primary aphakia in humans.

There is a keratolenticular adhesion (white arrow) (a and b seen with RetCam; courtesy of Leslie MacKeen), which causes a discrete CCO clinically and is seen on HFU (c). Histopathological examination of two cases of anterior staphyloma associated with Peters' anomaly and persistent hyperplastic primary vitreous.
This shows the mildest end of the spectrum of keratolenticular adhesion with iridocorneal adhesion. In a unilateral and otherwise healthy eye, it is difficult to explain this from a genetic developmental point.The characteristic feature of such mechanical touches is a lack of corneal vascularization (Figures 10, 12 and 13).
Again the distinction is important because synechiolysis or peeling off the keratolenticular adhesion with heavy viscoelastic may result in a focal discrete lens opacity and corneal scar.
The prognosis for penetrating keratoplasty in such cases is reduced only if there is exposure of the vitreous to the donor endothelium; in other words, if a vitreo-lensectomy needs to be performed at the time of penetrating keratoplasty. The picture below is that of a child with bilateral CCO who has HFU proven aniridia (in the undilated state!) with glaucoma. Compare this figure to Figure 9; here there is iridocorneal adhesion but no disruption of the iris stroma. Mutations at the PAX6 locus are found in heterogeneous anterior segment malformations including Peters' anomaly. The HFU evaluation shows disruption of the lens and iris, suggesting that this is likely to be failure of the lens to form properly although it appears from the HFU that it has separated from the cornea. Embryologically this makes sense because the lens vesicle induces basal ectodermal cells to form a multilayered structure, the cells of which increase in size and secrete the primary stroma. Although it has been thought that the infection is acquired during passage through the birth canal, cases have been described where the mother has found to be negative on microbiological evaluation.32 Both HSV type 1 and 2 have been implicated. The prognosis may be poor mainly because of the amblyopic effect in the first few weeks of life.
A family with Axenfeld–Rieger syndrome and Peters anomaly caused by a point mutation (Phe112Ser) in the FOXC1 gene. The infant often needs an examination under anaesthetic for corneal valuation corneal scrapes. The infant needs a full paediatric review as the ocular condition may be the only manifestation of a systemic infection including hepatitis and early encephalitis.
Under such circumstances penetrating keratoplasty is necessary to aid visual rehabilitation after adequate control of the glaucoma. Chromosomal anomalies are more likely in this group and in those cases with other organ or system anomalies.Developmental anomalies of the adnexaThe best example of this is in clefting syndromes where the cleft involves the globe and results in a secondary CCO usually with disruption of the anterior segment (Figure 18).
It seems that we are unclear by using these terms, which have served us well for at least 100 years, about the phenotype that is being described.

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