Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

New perfilcon contact lenses (71% water) were placed on one eye of 36 rabbits under complete tarsorrhaphy for 7 days. The lenses were then removed, and 18 were incubated for 1 hour with a suspension of 1 x 10(8) colony-forming units per milliliter of Pseudomonas aeruginosa and replaced on their respective corneas. The remaining 18 eyes were inoculated with 0.1 mL of the P aeruginosa suspension; the lenses were not replaced. All eyes were again closed by tarsorrhaphy for 4, 8, 16, 24, 36 , or 48 hours. Ulcerative keratitis occurred in contact lens-wearing eyes only, as P aeruginosa penetrated the epithelium at 8 to 36 hours, and polymorphonuclear leukocyte migration began at 24 hours. Compared with conventional abrasion-wound models, the time course of infectious keratitis in this model was delayed, possibly due to less preexisting corneal trauma, but our findings suggest that soft contact lens wear facilitates bacterial invasion and also inhibits the host inflammatory response.
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PMID:Time course of experimental Pseudomonas aeruginosa keratitis in contact lens overwear. 211 65

Extended wear soft contact lenses are associated with an increased incidence of Pseudomonas aeruginosa keratitis. Because the first step in the pathogenesis of this disease is adherence of the microorganism to the corneal surface, we studied the effect of soft contact lens wear on the adherence of P. aeruginosa to the cornea. Rabbits were fitted for extended wear soft contact lenses in the left eye, and the right eye served as a control. Both eyes were then closed with a partial tarsorrhaphy. After 1-5 days of wear, the lenses were removed and the corneas of the left and right eye were removed. Differences in the number of adherent Pseudomonas and in lectin binding to lens-wearing corneas and non-lens-wearing corneas were determined. After 1, 3, and 5 days of soft contact lens wear, there was a significant increase in the number of P. aeruginosa adherent to the lens-wearing cornea. Three to eight times as many bacteria adhered to the lens-wearing eye as compared with the control eye (p less than 0.05). In addition, a soft contact lens placed in the eye followed by the immediate application of P. aeruginosa resulted in an eightfold increase in adherence of bacteria to the lens-wearing cornea (p less than 0.05). Lens wear also led to an increase in binding of concanavalin A (Con A), wheat germ agglutinin (WGA), and Maclura pomifera agglutinin (MPA) to surface epithelium covered by the lens. These corneal epithelial changes induced by extended wear soft contact lenses may provide some insight as to why soft contact lens wearers are predisposed to Pseudomonas keratitis.
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PMID:Contact lens wear enhances adherence of Pseudomonas aeruginosa and binding of lectins to the cornea. 211 22

Microbial adherence to corneal epithelial cells is the initial step in the development of infectious keratitis. In an attempt to inhibit this process, we evaluated the effects of concanavalin A (Con A) upon the adherence of Pseudomonas aeruginosa to injured rabbit corneal epithelial cells. A sterile 21-gauge needle was used to create linear epithelial injuries. Identical samples from suspensions of a pure strain of P. aeruginosa were placed on two groups of injured corneas. Prior to bacterial application, one group of corneas received topical application of Con A, a lectin that is capable of binding to alpha-D-mannose or alpha-D-glucose. The animals were sacrificed 1 hour after application of the bacteria. Scanning electron microscopy of the excised corneas revealed that, compared to the corneas that had not been exposed to Con A, those exposed to the lectin had significant fewer adherent P. aeruginosa bacilli. Additionally, only rare bacteria were noted adhering to the uninjured superficial epithelial cells. These results suggest that, by competitively binding to the exposed mannose and/or glucose groups on the surfaces of these cells, Con A is capable of inhibiting the adherence of P. aeruginosa to injured epithelial cells.
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PMID:The use of concanavalin A to competitively inhibit Pseudomonas aeruginosa adherence to rabbit corneal epithelium. 211 42

Adherence of bacteria to the corneal epithelium is the first step in the pathogenesis of corneal infection. Keratitis caused by Pseudomonas aeruginosa usually occurs among the contact lens wearers. Adherence of Pseudomonas aeruginosa to rabbit corneal epithelium, damaged by one week of hard contact lens wear, was examined histologically. The cornea was excised for scanning electron microscopy at 5, 15, 30 and 60 minutes after inoculation of Pseudomonas aeruginosa (0.2 ml, 10(8)CFU/ml). Pseudomonas aeruginosa did not adhere to the intact corneal epithelium, but traumatized cornea provided a site for adherence. In rabbits in which the eyelid was opened by lid retractors, large numbers of organisms were observed adhering to the injured cornea mediated by ocular surface mucin. Thirty minutes after inoculation, the adherent bacteria began to penetrate the epithelial cells and surface mucin by the formation of pockets surrounding the organism.
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PMID:[Adherence of Pseudomonas aeruginosa to the rabbit corneal epithelium]. 211 20

We used a rabbit model to investigate the pathogenesis of soft contact lens-induced bacterial keratitis. Rabbit eyes underwent complete tarsorrhaphy for 7 days either with (group A, n = 14) or without (group B, n = 13) new sterile soft contact lenses. On day 7, an increase in mean corneal thickness (20.3% in group A and 17.2% in group B) was detected. New or rabbit-worn soft contact lenses were then inoculated with 10(7) colony-forming units of Pseudomonas aeruginosa or by 0.1 mL of P aeruginosa suspension. On day 9, conjunctival cultures of all eyes yielded P aeruginosa. Corneal infection developed in 11 of 14 eyes wearing new or worn, contaminated soft contact lenses. Bacterial keratitis did not develop in any of the 13 eyes inoculated with P aeruginosa suspension. Light and electron microscopy of infected eyes showed abundant polymorphonuclear neutrophils destroying the epithelium, basement membrane, and stroma. Few bacteria could be detected and only in the deep stroma. Since bacterial suspension alone caused no inflammation, soft contact lens-wear appears crucial to corneal infection in this model.
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PMID:Experimental Pseudomonas aeruginosa keratitis from extended wear of soft contact lenses. 212 Nov 23

The Pseudomonas aeruginosa slime-glycolipoprotein (GLP) is considered as one of the principal pathogenetical factors of the bacterium. A single dose of 100 micrograms of the P. aeruginosa slime-GLP was injected in rabbit corneas intrastromally. Light microscopy showed that 4 hours after the injection, polymorphonuclear leucocytes (PMNs) began to infiltrate the anterior stroma. 24 hours after the intrastromal injection, PMNs had infiltrated full corneal thickness followed by multiple absceses formation, loss of epithelial and endothelial cells, disorganisation of normal collagen fibres and hyperplasy of fibroblasts. These morphological observations are very similar to those observed during experimental P. aeruginosa keratitis and show that the P. aeruginosa slime-GLP is at least in part responsible for the characteristic liquefaction necrosis of the keratitis induced by the P. aeruginosa.
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PMID:[Histologic study of corneal lesions caused by the slime-GLP glycolipoprotein of Pseudomonas aeruginosa]. 212 33

Pseudomonas aeruginosa elastase is a zinc metalloproteinase which is released during P. aeruginosa infections. Pseudomonas keratitis, which occurs following contact lens-induced corneal trauma, can lead to rapid, liquefactive necrosis of the cornea. This destruction has been attributed to the release of both host-derived enzymes and the bacterial products P. aeruginosa elastase, alkaline protease, exotoxin A, and lipopolysaccharide endotoxin. A synthetic metalloproteinase inhibitor, HSCH2 (DL)CH[CH2CH(CH3)2]CO-Phe-Ala-NH2, which we previously showed to be a potent inhibitor of corneal collagenase and alkali-induced corneal ulceration, was tested as a potential inhibitor of P. aeruginosa elastase. Inhibition constants (Kis) for the resolved diastereomers were determined with the chromogenic substrate furylacryloyl-glycyl-L-leucyl-L-alanine. One isomer had a Ki of 0.3 microM, while the other had a Ki of 0.4 microM. The more potent diastereomer was evaluated in vivo in experimentally induced Pseudomonas keratitis in rabbits. Following inoculation of one cornea of each rabbit, topical treatment with a 1 mM solution of the inhibitor significantly delayed the onset of corneal melting and perforation, as compared with the results for the control and gentamicin-treated groups. This protective effect suggests that the inhibitor may have a therapeutic application by delaying the progression of corneal destruction in Pseudomonas keratitis.
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PMID:Inhibition of Pseudomonas aeruginosa elastase and Pseudomonas keratitis using a thiol-based peptide. 212 41

Microbial keratitis with Pseudomonas aeruginosa is the most common corneal infection associated with contact lenses (CLs). Pseudomonas organisms are ubiquitous in nature, and can colonize CLs without a prior breach in lens care or hygiene. Although poor lens care is often found in affected patients, lens contamination and traumatic epithelial defects are more relevant. Hydrophilic lenses, particularly extended wear lenses, have been associated with a greater frequency of Pseudomonas keratitis. The polymer matrix of these lenses is apparently suited to the avid adherence of Pseudomonas organisms. Adherence is promoted by the presence of lens coatings, which begin to accumulate upon lens insertion and whose level mounts over time. Evidence suggests that infection is more common with mucin-coated contaminated CLs than with noncoated contaminated CLs. In general, lens wear can promote bacterial adherence to the ocular surface by shielding the cornea from the wiping action of the eyelids and immune components in tears. Still, experimental models have shown that keratitis develops regularly (84%) only in corneas that have been traumatized. Trauma may arise through lens insertion or removal, deposits or debris entrapment, hypoxia, or toxic reactions to solution preservatives. Extended wear is believed to facilitate the infectious process because of the chronic accumulation of coatings, the chronic exposure of CLs to potentially adherent bacteria, the continuous presence of irritating lens deposits, the prolonged entrapment of debris beneath the lens, and the relative infrequency of lens cleaning and disinfection.
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PMID:Pseudomonas keratitis and contact lens wear: the lens/eye is at fault. 218 78

Studies using ciprofloxacin for the therapy of experimental aminoglycoside-resistant keratitis caused by Pseudomonas aeruginosa were conducted using transcorneal iontophoresis as the drug-delivery system. Corneas infected with P. aeruginosa ATCC 27853/pMG6 were treated 22 hours postinfection with ciprofloxacin delivered by iontophoresis (0.8 mA X 10 min), mock iontophoresis (eyecup with no current), or frequently applied topical drops. Iontophoresis of 10 mg/ml or 25 mg/ml of ciprofloxacin significantly reduced the number of viable bacteria per cornea by more than 5 log units compared with untreated controls (P less than 0.0001). Five hours after the initiation of treatment, mock iontophoresis (10 mg/ml or 25 mg/ml) or 11 applications of topical ciproflaxicin drops (7.5 mg/ml) decreased the viable bacteria relative to the untreated controls by 5 log units (P less than 0.0001). One treatment with an eyecup was as effective as 11 treatments with topical drops (P greater than 0.75). One hour after treatment with iontophoresis or mock iontophoresis of 10 mg/ml of ciprofloxacin, aqueous humor concentrations were 83.75 +/- 8.85 micrograms/ml and 24.87 +/- 4.0 micrograms/ml (mean +/- standard error of the mean), respectively. One hour after the last of five applications of 7.5 mg/ml of ciprofloxacin (every 15 min for 1 hr) the aqueous humor concentration was 4.2 +/- 1.14 micrograms/ml. These results show the value of ciprofloxacin in treating aminoglycoside-resistant infections caused by P. aeruginosa and suggest that ciprofloxacin can be efficiently delivered by iontophoresis.
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PMID:Ciprofloxacin iontophoresis for aminoglycoside-resistant pseudomonal keratitis. 221 Sep 88

Transmission of herpes zoster infection from one sister to the other is described, resultant from close everyday contacts. Clinical manifestations of the disease (severity, dissemination, course and type of involvement) were much more marked in the elder sister, suffering from disseminated Darier's dyskeratosis and marked debility. Herpes was complicated with vasculitis, necrosis, Pseudomonas aeruginosa infection, development of pneumonia and keratitis. Problems of treatment of such patients are discussed.
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PMID:[Herpes zoster in 2 sisters]. 225 85


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