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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Different manifestations on some ocular and adnexal structures may accompany ichthyosis. Some ophthalmological manifestations in the clinical course of ichthyosis may endanger the eye and even lead to the sight loss. The paper reports a case of a patient with congenital ichthyosiform erythrodermia and ophthalmological manifestations on the lids and cornea. In addition to ichthyosis of the lid skin, squamous blepharitis and cicatricial ectropium of the lower lids were also present, while signs of exposure keratitis on the right eye and corneal leucostaphyloma on the left eye were also noted. Presence of lagophthalmos and permanent exposure of both eyeballs led to deterioration of the condition which may result in the sight loss on the right eye, as well. Therefore, contracture release of both lower lids was performed followed by full-thickness skin graft. Surgical procedure and the postoperative course were uneventful. The operation successfully corrected position of the lower lids and enabled formation and reestablishment of the precorneal tears film which led to improvement of the condition of the cornea. The effect has been maintained for six postoperative years now.
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PMID:[Ophthalmologic manifestations in patients with ichthyosis]. 130 16

An 81-year-old man with metastatic prostate carcinoma underwent a penetrating keratoplasty for phlyctenular keratitis. Two years later he developed a fleshy, vascular mass in the superotemporal corneal graft wound, at the site of prior graft sutures. An excisional biopsy of the mass was performed to rule out metastatic carcinoma. Histopathological findings were consistent with pyogenic granuloma. To our knowledge there have been no prior case reports illustrating pyogenic granuloma as a late complication of penetrating keratoplasty.
Cornea 1992 Nov
PMID:Pyogenic granuloma of the cornea after penetrating keratoplasty. 833 68

Collagen shields applied to the corneas of patients with bacterial keratitis degrade rapidly, often within a few hours. Once treatment brings the infection under control, subsequently applied collagen shields degrade more slowly. In vitro models were established to evaluate the significance of these observations. Twenty-four and 72-hour collagen shields were incubated with collagenase from Clostridium histolyticum. The in vitro rate of digestion of the shields was directly proportional to the concentration of collagenase, with the rate of digestion of the 24-hour shields being greater than that of the 72-hour shields. Therefore, the rate of collagen shield degradation may be a clinically useful index of collagenase activity on the ocular surface. Ultrastructural studies of collagen shields from patients with acute bacterial keratitis revealed irregular degradation of shield matrix with no evidence of adherence of microorganisms or inflammatory cells. Co-incubation of deepithelialized rabbit corneas and collagen shields resulted in inhibition of the digestion of the rabbit corneas when the weight:weight ratio of collagen shield:rabbit cornea was increased to greater than or equal to 2:1. Collagen shields may inhibit corneal collagen degradation in infectious ulceration and melting disorders by effectively competing for collagenase on the ocular surface.
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PMID:The collagen shield as a collagenase inhibitor and clinical indicator of collagenase activity on the ocular surface. 131 47

The protective effects of passive immunization with two kinds of anti-glycoprotein D (anti-gD) monoclonal antibodies, having different antiviral activities, were investigated in murine herpetic keratitis. One monoclonal antibody, designated M1, had high virus-neutralizing antibody titers, along with undetectable levels of complement-dependent cytolysis (CDC) and antibody-dependent cellular cytotoxicity (ADCC); the other, designated M12, exhibited extremely low titers of virus-neutralization with high level of CDC and ADCC. When systemically administered 24 hours prior to virus inoculation to the cornea, both M1 and M12 almost completely prevented the development of stromal keratitis. The protective efficacy of both was observed to be dose-dependent. Pepsin-treated M1 retained its efficacy in suppressing stromal keratitis, whereas pepsin-treated M12 did not. When the administration of M1 and M12 were delayed, both provided significant (but less complete) protection, up to 24 hours after virus inoculation. These results suggest that both virus neutralization and CDC/ADCC play an important role in preventing virus growth in the corneal stroma during the early stage of corneal infection.
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PMID:Protective effects of anti-glycoprotein D monoclonal antibodies in murine herpetic keratitis. 131 53

This study was aimed at investigating the changes occurring in superficial corneal epithelium (localized or diffuse, dotted or linear) as observed in 300 eyes after macrodacryography with iodate contrast media (iodized oil and water soluble non-ionic agents). In our opinion, the causes of iatrogenic short-life keratitis are: needle injury, the deposition of iodate contrast medium on the cornea and the reduction of palpebral winking, favoring dry eye, due to superficial anesthesia. The pharmacologic protection of the cornea by means of high-viscosity drugs allows both the number and the degree of keratitis to be markedly reduced. Therefore, contrast media must be chosen on the basis of anamnestic and clinical data, as well as of patient's symptoms, focusing mainly on the characteristics of the various agents--i.e., density, concentration, viscosity.
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PMID:[Causes and incidence of short-life keratitis caused by dacryography. Optimization of protective parameters]. 132 65

Recurrences of herpetic stromal keratitis are believed to be initiated by reactivation of herpes simplex virus infection, probably in the trigeminal ganglion. Genetic features of the virus and the host as well as the immune status of the host influence the outcome of infection. Following infection on the snout with HSV-1, mice with normal corneas usually develop mild anterior segment disease. We studied the induction of herpetic infection in mice that had abnormal corneas, containing center due to trauma or a spontaneous dystrophy. The corneal abnormality led to more frequent herpetic stromal keratitis and more severe anterior chamber reaction. In addition, we found that snout-infected mice with dystrophic corneas had an increased risk of dying from viral infection. Our data suggest that not only the strain of virus and the genetic background of the mouse, but also the state of the cornea itself, can contribute to susceptibility to ocular herpes infection.
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PMID:Presence of Langerhans cells in the central cornea linked to the development of ocular herpes in mice. 132 20

Although varicella is one of the most common infectious diseases in the United States, systemic and ocular complications are rare. We report a patient who developed disciform edema followed by microdendritic keratitis 1 and 2 months, respectively, after resolution of the acute phase of varicella. Cultures were negative, but serologic analysis found positive antibodies against varicella zoster virus and negative antibodies against herpes simplex virus. Based on this case and on a review of the literature, we believe that this delayed onset of keratitis represents a distinct category of varicella corneal complications.
Cornea 1992 Sep
PMID:Delayed onset of varicella keratitis. 133 Apr 39

To investigate the role of T cell subsets in the development of herpetic stromal keratitis (HSK) in a well defined model, we used an adoptive transfer approach in which thymectomized and T cell-depleted mice [T(-)] were reconstituted with different numbers of syngeneic immune T lymphocytes after topical corneal challenge with RE strain of herpes simplex virus-1. In vitro stimulated or unstimulated immune T cells obtained from cervical and retropharyngeal lymph nodes of mice with HSK were used in adoptive transfer experiments. Although T(-) mice developed an initial epithelial inflammation, stromal keratitis did not occur. Reconstitution experiments revealed that mice that received 2 x 10(7) or more unfractionated immune T cells could develop HSK lesions with severity comparable to immuno-competent control mice. In mice receiving CD8(+)-depleted populations, even fewer cells (5 x 10(6)/mouse) were able to induce significant HSK. In contrast, mice that received similar or increased numbers of cells depleted of CD4+ T lymphocytes did not develop HSK. Immune T lymphocytes transferred to mice that were mock infected on the cornea did not develop HSK, indicating that the immunopathogenic cells were virus specific and not merely reacting to autoantigens. Histopathologic examination of the diseased corneas demonstrated that the stromal inflammation in euthymic normal and T(-)-reconstituted mice was characterized by extensive polymorphonuclear leukocyte infiltration. Scattered lymphocytes, and occasional macrophages also were observed. These results provide further evidence that HSK represents an immunopathologic process mediated mainly by CD4+ T cells.
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PMID:Herpetic stromal keratitis: an immunopathologic disease mediated by CD4+ T lymphocytes. 135 75

Herpetic stromal keratitis (HSK) appears to represent an immunopathologic response in the cornea of the eye to HSV-1. T cells of the CD4+ subset were shown to be involved in the mediation of HSK, but how they subserve an immunopathologic role is uncertain. In the present report, we have isolated cells from eyes in the active phase of HSK and studied their cytokine profile after culture in vitro or stimulation with Ag or nonspecific mitogens. Inflammatory cells recovered from eyes consist of polymorphonuclear leukocytes, macrophages, and lymphocytes. As reported before, all the lymphocyte recovered were of the CD4+ phenotype. After stimulation in vitro with Ag or mitogen the cytokines IL-2, IFN-gamma, and TNF-alpha/beta were produced, but not the cytokines IL-4 and IL-10. Thus, on the basis of cytokine profile, ocular lymphocytes were identified as Th1 cells. Ocular cells were also stimulated with PMA and shown to produce IL-1. The results were discussed in terms of the possible means by which the Th1 cells induce tissue damage in HSK as well as in terms of the possible means by which a preferential accumulation of Th1 cell occurs in the eye.
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PMID:Predominance of Th1 cells in ocular tissues during herpetic stromal keratitis. 135 34

A rabbit model of Staphylococcus aureus keratitis was developed to study the chemotherapeutic efficacy of ciprofloxacin, vancomycin, and cefazolin. Intrastromal injection of 100 colony forming units of log phase S. aureus ATCC strain 25923 resulted in rapid growth in the cornea, peaking at 10(7) cfu/cornea by 12 hr post-infection. Slit-lamp examination revealed that infected eyes reached 30% of maximum inflammation by 10 hr and 60% by 22 hr post-infection. Antibiotic therapy (one drop every 15 min for 5 hr) was initiated at 4 hr post-infection (experiment 1) or 10 hr post-infection (experiment 2). Another group was initiated at 10 hr post-infection and treated for 10 hr (experiment 3). In experiment 1, treatment from 4-9 hr post-infection with 0.3% ciprofloxacin drops decreased the cfu per cornea 6.1 logs, compared to placebo-treated controls (P = 0.0001), and rendered 50% of inoculated eyes sterile. Vancomycin (5.0%) and cefazolin (5.0%) each lowered the cfu per cornea 4.6 logs (P = 0.0187) but did not sterilize any eyes. In experiment 2, therapy from 10-15 hr post-infection with 0.3% ciprofloxacin reduced the cfu per cornea 0.9 logs (P = 0.0001). Vancomycin (5.0%) and cefazolin (5.0%) decreased the cfu per cornea 0.2 logs (P = 0.3973) and 0.3 logs (P = 0.1307), respectively. In experiment 3, therapy from 10-20 hr post-infection with 0.3% ciprofloxacin reduced the cfu per cornea 3.9 logs (P < 0.0001). In this keratitis model, ciprofloxacin was more effective than vancomycin or cefazolin in killing S. aureus.
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PMID:Topical antibiotic therapy for the treatment of experimental Staphylococcus aureus keratitis. 139 5


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