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Recovery of Virus From Affected Infants

FREDERICK H. ROY, MD; ROGER L. HIATT, MD; SHELDON B. KORONES, MD; JACK ROANE, MD

Arch Ophthalmol. 1966;75(5):601-607.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

The congenital rubella syndrome is a welldescribed clinical entity. Gregg of Australia in 1941 first described congenital malformations following maternal rubella cases.¹ These defects included small, malnourished infants with unilateral or bilateral cataracts, sluggish pupillary response to light, nystagmus in the older babies, corneal haze that cleared, microphthalmus, heart lesions (usually patent ductus arteriosus), and an intolerance to atropine. This work was reviewed for the American ophthalmic literature by Reese in 1944.²

Charles Swan of Australia confirmed these observations in 1943 and also extended the spectrum to include deaf-mutism, cardiac defects without apparent ophthalmic defects, and microcephaly.³ Evans in 1944 first described tooth abnormalities consisting of retarded eruption and hypoplasia of the tooth enamel.⁴ Bruce Hamilton and associates⁵ in 1948 and Morlet⁶ in 1949 reported associated pigmentation of the retina in eyes without cataracts. Lundstrom in 1962 confirmed the above observations and found significant . . . [Full Text PDF of this Article]

Author Affiliations
Memphis

From the departments of surgery (ophthalmology) and pediatrics of the University of Tennessee Medical Units, Memphis.

Footnotes
Submitted for publication Sept 20, 1965.

Reprint requests to 858 Madison Ave, Memphis, Tenn 38103 (Dr. Roy).

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