Isolation of bacteriophages specific to a fish pathogen, Pseudomonas plecoglossicida, as a candidate for disease control.

Two types of bacteriophage specific to Pseudomonas plecoglossicida, the causative agent of bacterial hemorrhagic ascites disease in cultured ayu fish (Plecoglossus altivelis), were isolated from diseased ayu and the rearing pond water. One type of phage, which formed small plaques, was tentatively classified as a member of the family Myoviridae, and the other type, which formed large plaques, was classified as a member of the family Podoviridae. All 27 strains of P. plecoglossicida examined, which were isolated from diseased ayu from geographically different areas in 1991 to 1999, exhibited quite similar sensitivities to either type of phage. One strain of P. plecoglossicida was highly virulent for ayu, and the 50% lethal dose (LD(50)) when intramuscular injection was used was 10(1.2) CFU fish(-1); in contrast, phage-resistant variants of this organism were less virulent (LD(50), >10(4) CFU fish(-1)). Oral administration of phage-impregnated feed to ayu resulted in protection against experimental infection with P. plecoglossicida. After oral administration of P. plecoglossicida cells of this bacterium were always detected in the kidneys of control fish that did not receive the phage treatment, while the cells quickly disappeared from the phage-treated fish. Bacterial growth in freshwater was lower in the presence of phage, and the number of phage PFU increased rapidly. These results suggest that it may be possible to use phage to control the disease caused by P. plecoglossicida.

[The mechanism of corneal epithelial disorder induced by prostaglandin F2 alpha isopropyl unoprostone].

Deleterious effects of isopropyl unoprostone (PG-F2 alpha) on the ocular surface were evaluated using the in vivo barrier function assay of corneal epithelial cells and the proliferation assay of human corneal epithelial cells in vitro. The barrier function of corneal epithelial cells in vivo was not impaired by treatment with PGF2 alpha, but it was significantly suppressed by timolol. The result of cell proliferation assay of human corneal cells showed that the 0.12% PGF2 alpha ophthalmic solution caused greater suppression of cell proliferation and acuter cell toxicity than 0.5% timolol ophthalmic solution. Further study showed that not the vehicle but the PGF2 alpha itself was responsible for these deleterious effects. We conclude that the 0.12% PGF2 alpha ophthalmic solution affects cell migration and proliferation but not the barrier effects of the ocular surface. These results suggest that the corneal epithelial defect of glaucoma patients may be caused by these two independent mechanisms, namely suppression of cell proliferation by PGF2 alpha and the destruction of the barrier function of the ocular surface by timolol.

[Effect of systemic calcium antagonist on a model of ocular circulation disturbance induced by endothelin-1].

We studied the effect of generally applied calcium antagonist on endothelin (ET-1) treated rabbit eyes. Nicardipine (20 micrograms/kg) was injected intravenously 15 minutes before intravitreal injection of 10 microliters of ET-1 at 10(-6) M. We measured the relative caliber of the retinal artery (the caliber of the retinal artery at the edge of the optic nerve head (ONH)/that of ONH), the capillary blood flow in ONH, visual evoked potential (VEP), intraocular pressure (IOP), and blood pressure (BP). In the control group (0.4 ml/kg of saline), administration of ET-1 caused contraction of the retinal artery, decrease of the capillary blood flow in ONH, prolongation of the VEP latency, and reduction of IOP. But these effects were significantly reduced in the calcium antagonist group. These results showed that generally applied calcium antagonist inhibits the disturbance of ocular circulation induced by ET-1. However, it also caused significant reduction of BP until 45 minutes after application, so we will have to work to find the optimum dose of calcium antagonist.