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Introduction {#s1} ============ Posterior polymorphous corneal dystrophy (PPCD) is a rare bilateral disorder transmitted as an autosomal dominant trait. Clinically PPCD is characterized by vesicles, bands and polymorphous opacities with pathology at the level of Descemet membrane and the corneal endothelium. Peripheral anterior iris adhesions, iris atrophy, pupillary ectropion and corectopia may also develop. Occasional severe visual disability results from secondary glaucoma or corneal edema [@pone.0045495-Krachmer1]--[@pone.0045495-Laganowski1]. On ultrastructural examination, corneal endothelial cells show fibroblastic and epithelial-like transformation [@pone.0045495-deFelice1]--[@pone.0045495-Jirsova1]. The genetic heterogeneity of PPCD is currently known to be represented by three loci on chromosomes 20, 1, and 10 [@pone.0045495-Heon1]--[@pone.0045495-Gwilliam1]. PPCD1 (MIM ID \#122000) is located on 20p11.21. Mutation of the visual system homeobox gene 1 (*VSX1*; MIM ID \#605020) within this locus was reported as disease-causing in a few PPCD cases [@pone.0045495-Heon2], [@pone.0045495-Valleix1]. PPCD2 (MIM ID \#609140) is caused by mutation of the alpha-2 chain of type VIII collagen gene (*COL8A2*; MIM ID \#120252) located on 1p34.3-p32.3, however only one disease-causing mutation in one family has been described to date [@pone.0045495-Biswas1]. Mutations in the zinc finger E-box binding homeobox 1 gene (*ZEB1*; MIM ID \#189909) mapping to chromosome 10p11.2 were identified as disease-causing in PPCD3 (MIM ID \#609141) and it has been estimated that pathogenic changes within this gene account for approximately 25% of all PPCD cases, with a range from 9%--45% depending on population studied [@pone.0045495-Krafchak1]--[@pone.0045495-Vincent1]. We have previously shown that in two Czech families PPCD is linked to the short arm of chromosome 20, flanked by the markers D20S48 and D20S139 [@pone.0045495-Gwilliam1]. Exclusion of *VSX1* from this genetic interval by a linkage study, and lack of disease-causing changes, implies that an as yet undiscovered gene is causative for PPCD1 [@pone.0045495-Gwilliam1]. Families affected by rare dominantly inherited disorders are often unrelated, however occasionally they share a chromosomal genomic region implying that the pathogenic mutation arose in a common ancestor [@pone.0045495-Sherwin1]. In this study we observed that PPCD in the Czech Republic appears to have a remarkably high prevalence. A total of 19 Czech PPCD families, including two previously linked pedigrees [@pone.0045495-Gwilliam1], were ascertained and members of 17 pedigrees were genotyped for microsatellite markers spanning a region from 20p12.1 to 20q12. We correlated the observed haplotypes with geographical origin of the eldest family member known to suffer from the disorder and demonstrate that the high prevalence of PPCD in the Czech Republic is due to a common founder. Materials and Methods {#s2} ===================== Patients {#s2a} -------- The study was approved by the Ethics Committee of General University Hospital in Prague, Czech Republic and conformed to the tenets of the Declaration of Helsinki. All participants signed an informed consent prior to inclusion into the study. Subjects from 19 Czech pedigrees with familial PPCD were examined between the years 1995--2010 in the Department of Ophthalmology of the First Faculty of Medicine, Charles University in Prague. Ophthalmologic assessment included visual acuity, slit lamp examination, intraocular pressure measurements and specular microscopy using Noncon ROBO Pachy SP-9000 (Konan Medical Inc, Tokyo). Diagnosis of PPCD was