PubMed · 4274734
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H I Maibach, R B Stoughton. 1973. Topical corticosteroids.. https://doi.org/10.1016/s0025-7125(16)32226-x
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OBJECTIVE: To determine which antimicrobial agents were most effective against Pseudomonas sp-infected ulcerative keratitis, and identify any trends in the various clinical conditions associated with these bacteria that might assist in effective treatment of the disease. DESIGN: Retrospective case series. ANIMALS: 66 horses with 70 Pseudomonas sp-infected corneal ulcers. PROCEDURE: We reviewed medical records of horses admitted to the George D. Widener Hospital for Large Animals, University of Pennsylvania between July 1977 and December 1994. Records of horses that had Pseudomonas sp isolated from a corneal ulcer scraping or deep swab were included in the study. RESULTS: Aggressive topical medical treatment was successful in 57 ulcers and most likely would have been effective in 5 additional ulcers. Antimicrobial susceptibility testing indicated susceptibilities of 87, 85, and 93% to tobramycin, gentamicin, and amikacin, respectively. Although concurrent fungal infections were identified in only 2 of 35 ulcers examined, almost three fourths of the ulcers were treated with antifungal medications prophylactically. Clinical outcomes of the 70 affected eyes included: excellent vision with minimal leukoma, 73%; enucleation, 19%; blind phthisical eye, 4%; peripheral vision only, 3%; and euthanasia of newborn, 1%. CLINICAL IMPLICATIONS: Aggressive topical medication with microbial agents effective against Pseudomonas sp can result in excellent vision with minimal leukoma in most horses with corneal ulcers.
That terminals of uninjured primary sensory neurons terminating in the dorsal horn of the spinal cord can collaterally sprout was first suggested by Liu and Chambers (1958), but this has since been disputed. Recently, horseradish peroxidase conjugated to the B subunit of cholera toxin (B-HRP) and intracellular HRP injections have shown that sciatic nerve section or crush produces a long-lasting rearrangement in the organization of primary afferent central terminals, with A-fibers sprouting into lamina II, a region that normally receives only C-fiber input (Woolf et al., 1992). The mechanism of this A-fiber sprouting has been thought to involve injury-induced C-fiber transganglionic degeneration combined with myelinated A-fibers being conditioned into a regenerative growth state. In this study, we ask whether C-fiber degeneration and A-fiber conditioning are both necessary for the sprouting of A-fibers into lamina II. Local application of the C-fiber-specific neurotoxin capsaicin to the sciatic nerve has previously been shown to result in C-fiber damage and degenerative atrophy in lamina II. We have used B-HRP to transganglionically label A-fiber central terminals and have shown that 2 weeks after topical capsaicin treatment to the sciatic nerve, the pattern of B-HRP staining in the dorsal horn is indistinguishable from that seen after axotomy, with lamina II displaying novel staining in the identical region containing capsaicin-treated C-fiber central terminals. These results suggest that after C-fiber injury, uninjured A-fiber central terminals can collaterally sprout into lamina II of the dorsal horn. This phenomenon may help to explain the pain associated with C-fiber neuropathy.
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