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1984 21: 316Vet PatholS. D. Barkyoumb and H. W. Leipold

Nature and Cause of Bilateral Ocular Dermoids in Hereford Cattle

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Vet. Pathol. 21: 316-324 (1984)

Nature and Cause of Bilateral Ocular Dermoids in Hereford Cattle

S. D. BARKYOUMB and H. W. LEIPOLD

Department of Pathology, College of Veterinary Medicine, Kansas State University, Manhattan, KS

Abstract. Nature and cause of bilateral ocular dermoids were investigated by field studies, pedigree analysis, clinical examination, light microscopy, scanning electron microscopy, and transmission electron microscopy. It was determined that ocular dermoids in Hereford cattle are a genetically transmitted defect; characteristics of autosomal recessive and polygenic inheritance were observed. Calves typically were affected bilaterally with multiple, connected ocular growths that clinically, histologically, and ultrastructurally mimicked normal haired skin. Sites most commonly involved included ventro-lateral limbus, third eyelid, medial canthus, eyelid and conjunctiva. Centro-corneal and anterior segmental dermoids also were observed.

Ocular dermoids, as reported, are peculiar defects recognized in animals and man characterized by solid, skin-like masses of tissue on or in various ocular structures. Their cause is controversial?-6. Is. 20. 23. 25. 43* 51. 52

They occur sporadically in numerous cattle ave no

clear-cut sex incidence,'. 35 and occur unilaterally and bilaterally.6.9. 10. 12.24.34. 53 Ocular dermoids may be nothing more than a cosmetic blemish and a source of irritation which is removed easily by superficial lamellar

lar dermoids usually appear clinically as a singular mass adhered to the anterior surface of the globe astride the ventro-lateral limbus.'. 4. 12.41. 52 They may cause visual impairment if large areas of the cornea are involved. Dermoids involving central cornea, third eyelid, canthus or eyelid occasionally occur in cattle and are corrected easily by surgery. lo Total corneal replacement and anomalies of internal ocular structures have not been reported in association with ocular dermoids in cattle.

Recent reports to us from veterinarians from southcentral Iowa indicated a high incidence of ocular dermoids within individual Hereford herds. These cases were unique because calves were affected bilaterally with multiple dermoid growths per eye causing mod- erate to marked disfigurement of external ocular structures. In addition, small tissue masses protruding into the external nares and heart murmurs were reported in several calves. The overall objective of this study was to investigate the nature and cause of bilateral ocular dermoids in Hereford cattle.

breeds,3. 10. 16-18.25.32. 33. 35. 36. 40-42.47. 49. 53. 54 h

keratectomy with little resultant scamng.". I I . 15.29 ocu-

Materials and Methods

Initial reports of ocular dermoids received from local veterinarians, breed associations, extension personnel, and herd owners were recorded. Herds with ocular dermoids were visited or the owners contacted by telephone to determine if any adverse environmental factors were associated with ocular dermoids. The following factors were investigated breed, sex, degree of ocular involvement, age of parents, geographic region, season, type of pasture, soil type, exposure to or suspected exposure to teratogenic plants, feeding and man- agement practices, breeding records, maternal medical and vaccination records, disease status of the herd, periods of stress, drugs administered, congenital defects observed previ- ously, and history of similar congenital defects in neighboring herds.

Breeding records of defective calves were collected and complete pedigrees of at least five generations were con- structed for 23 purebred Polled Hereford calves affected with ocular dermoids. Pedigrees were compared with five generation pedigrees of 100 normal Polled Hereford calves of similar age and randomly selected from the computer records of the breed association to investigate the degree of similarity in ancestral background between abnormal and normal calves.

Sixteen calves with various grades of ocular dermoids were purchased and transported to Kansas State University for thorough examination. Upon amval the calves were examined clinically and photographed; unclotted blood samples for differential blood cell counts, clotted blood for blood chemistry profile (creatinine, glucose, inorganic phosphorus, calcium, albumin, total protein, alkaline phosphatase, blood urea nitrogen, carbon dioxide, potassium, sodium and chlo- ride), serum for detection of infectious bovine rhinotracheitis, bovine virus diarrhea and blue tongue viral antibodies, and heparinized whole blood for bluetongue virus isolation were collected.

Calves to be necropsied were anesthetized by intravenous sodium pentobarbital. Nasal and ocular swabs, samples of

3 16



Ocular Demoids in Herefords 3 17

Table I. Location, year of occurrence, breed, sex, and involvement of 74 calves with ocular dermoids Breed Sex Involvement

Un- Bi- Uni- Un- Farm Location Year ofcalves Number Polled Here- Homed Grade Here-

fords fords fords crosses Here- Here- ford Male known lateral lateral known with dermoids

A B C D E F

G

H I J K L

M N 0 P

Iowa 1981 Iowa 198 1 Iowa 1981 Iowa 1981 Iowa 1981 Iowa 1982

1981 1976

Iowa 1981 1976 1971

Iowa 1981 Iowa 1981 Michigan 198 1 Kansas 1981 Iowa 1981

1980 Iowa 1981 Iowa 1981 Iowa 1981 Kansas 1980 Total

2 6 3 7 6 4

15 4 2 2 I 4 I 1 1 3 1 6 2 2 1

74

0 0 0 0 0 4

12 0 0 0 0 3 0 1 0 1 1 0 0 1 0

23

0 0 0 6 0 3 0 7 0 6 0 0 0 3 0 4 0 2 0 2 1 0 0 1 0 1 0 0 0 1 2 0 0 0 0 0 0 2 0 1 0 1 3 40

2 0 1 0 0 0 0 6 0 3 0 0 0 1 0 7 0 1 0 5 0 3 1 0 0 7 7 1 0 0 0 4 0 2 0 0 0 0 0 2 0 0 1 0 0 4 0 0 0 1 0 0 0 1 0 0 0 1 0 0 0 1 2 0 0 0 1 0 6 2 2 2 0 1 1 0 0 2 0 0 0 1 0 0 8 31 16 27

2 0 0 6 0 0 3 0 0 6 1 0 6 0 0 3 1 0

14 1 0 0 0 4 2 0 0 0 0 2 0 I 0 4 0 0 1 0 0 0 1 0 1 0 0 3 0 0 1 0 0 6 0 0 1 1 0 2 0 0 1 0 0

62 6 6

aqueous humor and portions of dermoid and four nasal masses were taken for virus isolation. The jugular yeins were severed, the vascular system of the head was flushed with heparinized saline via the carotid arteries, and the head was fixed by intracarotid perfusion of Trump’s solution containing 4% phosphate buffered formaldehyde and 1 % glutaralde- hyde.”

Enucleated eyeballs, eyelids, intraorbital tissues, lacrimal glands, nasal masses and somatic tissues were placed in Trump’s solution for at least 72 hours. Samples for infectious bovine rhinotracheitis (trachea, lung, kidney) and bovine virus diarrhea (spleen, mesenteric lymph nodes, intestine and feces) virus isolation were collected.

Ocular tissues were embedded in paraffin, sectioned at 8 pm by a sliding microtome, and stained with hematoxylin and eosin (HE).” Nonocular tissues were cut at 6 pm on a rotary microtome and stained with HE.

Selected sections of dermoids were processed for scanning electron microscopy. A modified osmium thiocarbohydrazide procedure was used crosslinking layers of osmium to the tissue to render them conductive and prepare them for scanning electron micro~copy.~~

Following application of this technique, tissues were dehy- drated in increasing grades of ethanol, critical point dried with liquid COz, mounted on aluminum studs with colloidal silver paste, and examined by scanning electron microscopy.

Following scanning electron microscopic examination, selected samples of dermoid tissue were removed from the prepared blocks as described above and prepared for trans-

mission electron microscopy. Small minced fragments of tissue were infiltrated with and embedded in LX-112 resin (Ladd LX-112 Resin, Ladd Research Industries Inc, Burling- ton, VT) polymerized at 60°C for 12 hours. Thick sections (0.5 to 1 pm) were cut from each block, stained with toluidine blue, and examined by light microscope to confirm orienta- tion. Ultrathin sections (80 to 100 nm) were placed on a copper grid, stained with uranyl acetate and lead citrate, and examined by transmission electron microscope.

Results

Complete blood counts revealed various degrees of neutrophilia. Serum chemical constituents were normal. Serum viral antibody titers for .infectious bovine rhinotracheitis, bovine virus diarrhea and bluetongue and virus isolation studies conducted on blood, intraocular fluid, dermoid tissue, somatic tissue and nasal masses were negative.

Seventy-four calves with congenital ocular dermoids were reported in 16 different herds located in three states-7 1 from southcentral Iowa, two from northcen- tral Kansas, and one from Michigan (table I). Four calves were born in 1982, 61 in 1981, two in 1980, six in 1976, and one in 197 1. Breeding histories revealed 40 calves were grade Herefords, 23 were purebred Polled Herefords, three had purebred Horned Hereford



318 Barkyoumb and Leipold

parents, and eight were Hereford crossbreds. No other cattle breeds located in southcentral Iowa were affected. Thirty-one calves were male, 16 female, and the sex of 27 was not reported.

Parents were phenotypically normal except one bull and one cow. The bull had a thickened nodular third eyelid and the cow had a small speck involving the cornea of one eye. Sixty-two calves had dermoid growths affecting both eyes, six were unilateral, and involvement of six was not reported. There was marked variation in extent of dermoids which ranged from a small growth to marked ocular malformation with blindness.

No environmental factor could be associated with the ocular dermoids. One rancher indicated vitamin A deficiency ten years earlier and except for infectious keratoconjunctivitis in one herd, no significant viral or bacterial diseases were reported. The use of drugs or other medications in cows having calves with dermoids was not reported and vaccination schedules were routine. Solanum spp (Nightshade) was found to be a problem in one herd; a survey of the grazing areas of other herds, however, did not reveal any poisonous plants.

The 23 purebred Polled Hereford calves with ocular dermoids (1 5 male, seven female, and one unknown sex) had separate dams and were sired by seven different bulls; 15 calves were sired by one bull. The sire of this bull also sired a calf with a dermoid and a paternal grandsire of a bull reported to have sired a calf with a dermoid. Three defective calves were sired by a common bull, and the remaining three bulls sired one defective calf each.

Examination of five- to eight-generation pedigrees of affected calves revealed three common ancestors: bulls 1-1, 1-2, and 1-3. Twenty-two calves (96%) were related to bull I- 1 ; 18 calves were related through both sides of their pedigree (dam and sire), and four via their sire. His presence was established in only 16 (16%) of the 100 randomly selected five-generation pedigrees of normal calves of similar age. Bull 1-2 was present in 22 of the 23 pedigrees (96%); 15 through both parents, six through the sire only, and one through the dam. He occurred in 31 (31%) of the 100 randomly selected pedigrees. Bull 1-3 was in 22 of the affected (96%) and 42 (42%) of the randomly selected pedigrees. He occurred in the ancestors of both the dam and sire in 13 of the calves with dermoids, the sire of eight calves and the dam of one calf. It was noted that common ancestry of these bulls to randomly selected normal calves was usually through one parent only, not both.

There was considerable variation among individual eyes and between calves in expression of the defect depending on location, size, amount and type of hair, and number of skin-like masses present. Most calves were affected bilaterally with multiple, connected ocular dermoids resulting in mild to marked disfigurement of cornea, canthi, and eyelids. There was encroachment on the visual axis with various degrees of visual impairment, and significant subacute keratoconjunctivitis with epiphora, blepharospasm, and corneal ulceration. Inflammation was related directly to imtation by the dermoid and to exposure keratitis secondary to eyelid dysfunction. Defects of the heart (tetralogy of Fallot, patent ductus arteriosus), kidney (polycystic) and nasal cavity (masses protruding into nares) were observed in some calves.

Sites most commonly affected in decreasing order of incidence included limbus, third eyelid, canthus, eyelid, and conjunctiva (table 11). Dermoids strictly of lacrimal caruncle and dermolipomas of the conjunctiva were not observed. Limbal dermoids (figs. 1-3) occurred most frequently astride the ventro-lateral, corneo- scleral junction and canthal dermoids involved primarily the medial canthus. Centro-corneal dermoids (figs. 4-6) and anterior segmental dermoids (figs. 7-9) with complete corneal replacement and marked dysplasia of internal ocular structures also were observed.

Variation within and among the numerous dermoids observed histologically and ultrastructurally included epidermal thickness, degree of epidermal keratinization and pigmentation, prominence of rete pegs and dermal papillae, degree of subacute subepidermal inflammation, number of epidermal adnexa, dermal thickness, amount of adipose tissue in subcutis, tightness of dermoid-corneal/scleral junction, and depth of corneal replacement. Subacute subepidermal, conjunctival, and corneal inflammation were observed in all dermoids and adherent intradermal lacrimal tissue frequently was present in deeper dermoid layers. Anterior segmental dermoids contained fascicles of skeletal muscle and bands of hyaline cartilage. They were associated with sclero-cornea, aphakia, dysplasia of anterior uvea, scleral ectasia, retinal detachment and dysplasia, subretinal hemorrhage, persistent hyaloid artery, and co- loboma of the optic disc.

Discussion Limbal, centro-corneal, anterior segmental, conjunc-

tival and third eyelid dermoids were examples of cho- riostomatous growths because they clinically, histologically, and ultrastructurally resembled dystopic masses



Ocular Dermoids in Herefords 3 19

Table 11. Location of ocular dermoids in 16 Hereford cattle Left eye Right eye

Anter- Cen- Con- Third Can- Eye- ior tral Limb- junc- eye- Con- Third Can- Eye-

junc- eye- thus lid tiva lid thus lid seg- cor- us tiva lid

Calf Anter- Cen- number ior tral Limb-

seg- cor- us ment nea ment nea

1 1 2 0 3 0 4 0 5 0 6 0 7 0 8 0 9 0 LO 0 1 1 0 12 0 13 0 14 0 15 0 16 0

0 0 0 1 2 1 1 0 0 0 1 1 2 0 1 1 0 2 0 0 1 1 0 1 2 1 0 I 1 1 1 1 0 0 2 0 1 0 0 0 3 0 0 0 0 0 0 1 1 1 0 1 0 2 0 1 1 0 0 1 2 0 0 1 1 1 0 0 1 1 2 0 1 1 0 0 1 2 0 2 1 1 0 0 0 0 1 1 1 1 0 0 1 0 1 0 0 0 0 0 0 0 0 0 0 1 1 1 0 0 0 0 1 1 0 0 0 0 0 0 1 1 0 0 0 I 0 1 0 0 0 0 1 1 0 0 0 0 0 0 0 0 0 0 1 1 0 0 0 0 0 1 0 0 0 0 0 1 0 0 0 0 0 0 1 1 0 1 0 0 0 0 0 0 0 0 0 1 0 0 0 0 0 0 0 1 0 0 0 0 1 0 0 0 0 0 1 0 1 1 0 0 0 0 0 0 1 0

of normal skin. Canthal and palpebral dermoids were due to benign orderly overgrowth of mature cells and tissues present in the dermis of haired skin normally covering these ocular structures. Because these growths represented more of the same, they were classified as hamartomas.

Developmental mechanisms involved in pathogenesis of ocular dermoids are not known. Dermoids have been attributed to metaplasia of corneal epithelium secondary to excessive exposure of the cornea to the intrauterine environment caused by abnormal development and closure of the Other causes are adhesion and implantation of portions of am- nion,22. 48.50 plica semilunaris,14 attachment of eyelids to the corneal ~urface,’.’~ invagination of isolated islands of surface ectoderm capable of developing into skin and adnexaY3’ and abnormal differentiation of mesoderm lying between the optic cup and surface ectoderm.”. 31.43 Mesodermal metaplasia is the most plausible mechanism of development since surface ectoderm depends on underlying mesodermal tissues for differentiati~n.~’ Underlying mesoderm determines whether surface ectoderm forms nonkeratinized strati- fied squamous epithelium and Bowman’s membrane of the cornea or if it keratinizes and forms epidermal adnexa characteristic of haired skin. It is not known whether dermoids result from a primary aberration of invading corneogenic mesoderm, abnormal inductive influences from underlying vestiges of the embryonic

eye, or if there is sequestration of dermal tissues destined to induce haired skin formation.

Cornea forms from two germ layers, surface ectoderm and mesoderm, under inductive influences of the developing optic cup and lens vesicle. Without these influences, surface ectoderm and invading corneogenic mesoderm would develop into opaque vascular skin or opaque connective tissue indistinguishable from ~ c l e r a . ~ ~ Marked intraocular dysplasia, aphakia, and total replacement of cornea by scleral-like tissues and skin were observed in a calf with extensive bilateral anterior segmental dermoids. Therefore, abnormal inductive influences derived from dysplastic rudiments of the underlying embryonic eye may have contributed to ocular dermoid formation.

Corneal formation begins when the lens vesicle closes with the remaining surface ectoderm overlying the mouth of the optic cup giving rise to anterior corneal epithelium and its basal lamina. It is at this time that mesenchymal cells surrounding the optic cup migrate between the anterior surface of the lens vesicle and overlying anterior corneal epithelium. Infiltration of corneogenic tissues occurs in waves with the first wave resulting in formation of posterior corneal endothelium. Successive waves of invading mesenchyma form the substantia propria of the cornea-first posteriorly, then anteriorly.” If latter waves of invading mesenchyma contain sequestrations of cells destined to form the dermis of haired skin, it would be possible to have




3

6

Fig. 1: Ventro-lateral limbal(1) and palpebral (p) dermoids. Fig. 2: Eyeball of fig. 1. Ventro-lateral limbal dermoid (1) continuous ventrally with thickened nodular lower eyelid (p) and

dorsally with sheet of conjunctival tissue (con) attached to bulbar conjunctiva of opposite limbus. Fig. 3 Whole eye section of eye shown in fig. 2. Thick limbal dermoid closely adhered to cornea and continuous with

posterior aspect of lower eyelid (arrow). Band of conjunctival tissue connects dermoid with opposite limbus. HE. Bar = 1 cm. Fig. 4: Multiple dermoids involving medial canthus (mc), lower eyelid, and central cornea (cc). Fig. 5: Eyeball of dermoids shown in fig. 4. Large protruding centro-corneal mass of skin (cc) covered with dark hair. Fig. 6: Entire eye section of eyeball shown in fig. 5. Large protruding mass of skin adhered to anterior surface of cornea.

Extension over limbus (arrow) is minimal. HE. Bar = 1 cm.



Ocular Dermoids in Herefords 32 I

Fig. 7: Large mass of haired skin (as) involving anterior segment of eyeball and surrounding palpebral and canthal structures

Fig. 8: Sagittal section of dermoid shown in fig. 7. Fig. 9: Entire eye section of affected eye shown in figs. 7 and 8. Thick mass of haired skin covers anterior surface of the

globe. Globe affected with multiple developmental defects. Cartilage (crt), skeletal muscle (skm), replacement of cornea by sclero-cornea (scc), scleral ectasia (se), subretinal hemorrhage (sh), detachment of retina (ret), persistent hyaloid artery (pha), and infiltration of sclero-cornea by dysplastic uveal and retinal tissues (arrow). HE. Bar = I cm.

(arrows).

normal formation of posterior corneal endothelium and posterior aspects of the substantia propria with dermoids involving more superficial corneal layers.

It is not known where adherent mesoderm might arise. It was noted that pigment distribution in dermoids and texture of hair covering them was similar to surrounding eyelids and facial skin. One might hypoth- esize that the origin of ocular dermoids and skin of surrounding eyelids may be related. Eyelids develop from a fold of mesoderm covered on both sides by surface ectoderm that encircles the gradually protruding

eye at about the same time as the corneal epithelium and stromal mesenchyma are forming. As growth con- tinues, upper and lower portions of these folds extend toward each other, meet over the cornea in a horizontal plane and fuse by forming an epithelial seal. If islands of mesoderm destined to form palpebral skin become misdirected and invade beneath surface ectoderm in the process of differentiating into conjunctival or corneal epithelium, then dermoids would develop. De- pending upon how far adherent mesoderm migrates, dermoids could involve conjunctiva, limbus or central




cornea. Factors responsible for abnormal migration of palpebral mesoderm ‘also may be responsible for formation of third eyelid, palpebral and canthal dermoids.

Anterior segmental defects may result by combina- tion of two processes: abnormal inductive influences derived from dysplastic rudiments of the embryonic eye, and abnormal sequestration of palpebral mesoderm in the superficial layers of the sclero-cornea.

Because of its role in epithelial metaplasia and ability to produce microphthalmia and related ocular defects, hypovitaminosis A in utero has been incriminated as a possible initiating factor in development of adherent mesoderm between optic cup and surface e c t ~ d e r m . ’ ~ . ~ ~ Microphthalmia, dysplasia of internal ocular structures and hypoplasia of optic nerves were associated with anterior segmental dermoids. Deformation of sphenoid bones and stenosis of optic foramina, both characteristics of hypovitaminosis A in utero, were not observed; therefore, ocular dermoids were not considered to be secondary to a vitamin A deficiency in utero.

Localization of the defect primarily to southcentral Iowa could not be linked to any known teratogenic environmental influence although undetected environmental factors may have played a role in the sudden high incidence in 198 1 and in the variable phenotypic expression of ocular dermoids. It also is reasonable to suggest that regionally high incidence of ocular dermoids was related to the use of common breeding cattle between neighboring herds and surgical correction of minor dermoid growths in these cattle-which over a period of time resulted in an increasing pool of dermoid-producing genes.

In man, most congenital defects of the anterior segment of the eye are determined geneti~ally,~~ but the role of inheritance in ocular dermoids has been debated in animals4-6. 16.23.25.41.46.51 and man.’0.43.52 High incidence in Hereford cattle endogenous to southcentral Iowa without a concurrent increase in other breeds, bilateral expression of the defect, common ancestry suggesting familial tendencies, occurrence in males more than females, independence from season and inability to demonstrate any known teratogenic environmental influence suggested that ocular dermoids in cattle observed in this study may be transmitted genetically. The mode of genetic transmission of bilateral ocular dermoids in Hereford cattle was not established although characteristics of both autosomal recessive and polygenic inheritance were observed. Phenotypi- cally normal parents, common ancestral backgrounds, genetic isolation by geographic barriers, and sporadic occurrence of the defect in previous generations of some

herds indicated possible autosomal recessive inheritance for bovine ocular dermoids.

Examination of 23 affected and 100 randomly selected normal purebred Polled Hereford calves of similar age revealed the occurrence of three bulls with regular frequency in the pedigrees of affected calves. Common ancestry of normal calves to the same three bulls occurred less frequently and when present, it was usually through the dam or sire only, not both. Calves with dermoids, however, usually had the suspect sires on both sides of the pedigree, suggesting ocular dermoids may be the result of an autosomal recessive gene in the homozygous state, with one gene coming from each parent. If present in these common bulls, the defect could have been transmitted from generation to generation by phenotypically normal cattle or those corrected surgically, resulting in insidious spread of dermoid genes in the cattle population localized geo- graphically in southcentral Iowa.

Multifactorial polygenic inheritance involving addi- tive effects of many minor genes and subtle environmental influences is the most common cause of hereditary defects of a localized nature in man.” Simulation of autosomal recessive inheritance, variable expression of the dermoid defect, tendency to occur more in males than females, possible subtle environmental influences endogenous to southcentral Iowa, low rate of recurrence in affected herds, and common ancestry of affected cattle would be consistent with but not proof of polygenic inheritance of bovine ocular dermoids.

It is postulated from this study that bilateral ocular dermoids are genetically transmitted defects in Here- ford cattle. Characteristics of both autosomal recessive26 and polygenic inheritance were observed; however, mode of inheritance and role of environment in the pathogenesis of these peculiar and important developmental defects remain undefined. Extensive breeding trials utilizing superovulation, embryo transfer, and preterminal caesarean section as well as further field studies will be necessary to confirm sex incidence, significance of associated somatic defects, role of environment in phenotypic expression, and mode of transmission of ocular dermoids in Hereford cattle.

Ack.nowledgement This research was part of the Regional Project NC-2.

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Ocular Derma ids in Herefords 323

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Request reprints from Dr. H. W. Leipold, Department of Pathology, College of Veterinary Medicine, Kansas State University, Manhattan, KS 66506 (USA).



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