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Topical vancomycin formulation for methicillin-resistant Staphylococcus epidermidis blepharoconjunctivitis.

A B Fleischer·D L Hoover·J A Khan·J T Parisi·R P Burns
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Abstract

We successfully treated two patients with severe Staphylococcus epidermidis blepharoconjunctivitis by means of a topical vancomycin hydrochloride solution (50 mg/ml) prepared with sterile water. Aqueous vancomycin preparations, however, cause significant ocular irritation probably because of low pH and osmolality values. Solutions prepared with normal saline (5 mg/ml) and phosphate-buffered artificial tears (5 mg/ml and 50 mg/ml) were significantly less irritating and possessed equivalent in vitro antimicrobial activity. Topical vancomycin should be used only when commercially available antibiotics are inadequate.

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Administration, TopicalAgedBlepharitisConjunctivitisDrug EvaluationEyelid DiseasesHumansHydrogen-Ion ConcentrationMaleMethicillinOphthalmic SolutionsOsmolar ConcentrationPenicillin ResistanceStaphylococcal InfectionsStaphylococcus epidermidisVancomycinCase ReportsJournal ArticleResearch Support, Non-U.S. Gov't

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A B Fleischer, D L Hoover, J A Khan, J T Parisi, R P Burns. 1986-03-15. Topical vancomycin formulation for methicillin-resistant Staphylococcus epidermidis blepharoconjunctivitis.. https://doi.org/10.1016/0002-9394(86)90820-2

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PubMed1995

Removal of the majority of epidermal Langerhans cells by topical or systemic steroid application enhances the effector phase of murine contact hypersensitivity.

Whereas epidermal Langerhans cells (LC) are thought to be the principal APCs for initiation of contact hypersensitivity (CHS) responses, their role as APC in the effector phase of CHS is still unclear. It is currently thought that LC elicit the CHS response by presenting Ag to trafficking Ag-specific T cells within the skin. To test this hypothesis, we removed the majority of resident LC at the site of CHS challenge by topical application of various steroid creams to one ear in BALB/c mice (> 85% LC depletion). Either 2 days before or 4 days after steroid treatment of the ear, mice were sensitized on the abdomen with the hapten trinitrophenyl and challenged 10 days later at the steroid-pretreated ear. At that time point, direct anti-inflammatory effects of the steroid were no longer present. Surprisingly, CHS responses were markedly stronger at the sites of prior steroid application when compared with vehicle-treated controls, indicating that depletion of most of the resident LC not only fails to impair, but enhances, the expression of CHS significantly. UV irradiation or application of croton oil at the challenge site, as well as systemic steroid application, all of which are alternative methods of diminishing the number of epidermal LC, also significantly up-regulated CHS. In contrast, irritant dermatitis and sensitization or elicitation of CHS in steroid-treated mice at distant sites, as well as delayed-type hypersensitivity responses against the same hapten, were unaffected by topical steroid pretreatment. In conclusion, our data suggest that resident LC are not the relevant APC in the effector phase of CHS and that they may even provide down-regulatory, rather than stimulatory, signals during elicitation of CHS.

Administration, Topical↗