Is the Flu Related
To This Eye Condition?Mark T. Dunbar, O.D
A 21-year-old college student complained of blurry vision in his left eye for the past week and a half. About two weeks earlier he had a flu-like illness with severe headache, vomiting, fever, chills, lymphadenopathy and malaise. This lasted about a week. He was admitted to a hospital after the second day, where, as he put it, he underwent ďevery test under the sun,Ē including a CT-scan and lumbar puncture. He reported that all the tests were negative and that he was discharged after four days when his condition began improving. The doctors gave him no specific diagnosis. His vision problems began about a week later.
Best-corrected visual acuity was 20/20 O.D. and 20/60 O.S. Confrontation fields were full to careful finger counting. The pupils were equally round and reactive, and there was an afferent pupillary defect in the left eye. On Ishihara color plates he got 15/15 correct O.D., 6/15 O.S. The anterior segment was unremarkable in both eyes.
A dilated fundus exam of the right eye showed a small cup with good
rim color and perfusion. The remainder of the right eye was normal. The
left eye showed marked disc swelling and a macular star (see photos). Trace
cells were strewn throughout the vitreous. Along the superior arcade was
a small white intraretinal infiltrate resembling a cotton-wool spot.
Leberís idiopathic stellate neuroretinitis was characterized in 1916 by the German ophthalmologist Theodor Leber to describe a clinical syndrome of unilateral vision loss, optic disc swelling, macular star formation and spontaneous resolution.1 It was later discovered that as many as two of three patients had a preceding viral-like illness.2 Thus for many years this condition was classified as a post-viral neuroretinitis. Patients received little or no work-up because it usually revealed no definitive etiology.
As laboratory testing methods improved, cat-scratch disease (CSD) was
soon recognized as the cause for many patients with Leberís stellate
Usually children or young adults present with CSD. Often there is an
antecedent viral-like illness, which may be associated with a history of
a cat scratch. CSD has also been known to occur from a cat lick or from
handling objects associated with cats. Kittens seem to be especially viruliferous.
The hallmark of the disease is a neuroretinitis with exudate extending into the macula. The exudate is located between the outer plexiform and inner nuclear layers within the retina, forming a macular star.
For many years clinicians believed that neuroretinitis was the sole intraocular manifestation of cat-scratch disease. We now know that other findings can occur. Among these are small, multifocal, white lesions located within the inner retinal layers that likely represent areas of retinal ischemia. These can resemble cotton wool patches. In many patients these small white lesions have led to branch retinal artery occlusions.
The work-up for a patient suspected of having CSD should include the
indirect fluorescent antibody assay (ELISA) for Bartonella henselae, the
organism responsible for CSD. This test, available through the Centers
for Disease Control in Atlanta, can detect antibodies to cat-scratch bacillus.
Our patient had classic neuroretinitis from CSD. He also had one of
the characteristic white retinal lesions associated with the condition.
When questioned, he did say he had several cats. He couldnít recall a recent
scratch. He also spoke of the post-viral illness that led to hospitalization.
© Review of Optometry OnLine