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Biomedical subjects

E M Opremcak

Publications and source records attributed to E M Opremcak.

At least 19 recordsLinked to original sources
PubMed2001

Radial optic neurotomy for central retinal vein occlusion: a retrospective pilot study of 11 consecutive cases.

PURPOSE: Retinal vascular occlusive disease is the second leading cause of permanent retinal blindness. The etiology of central retinal vein occlusion (CRVO) is not well understood. The anatomy of the optic disk including the cribriform plate and scleral ring may contribute to the development of retinal vaso-oclussive diseases. Neurovascular compression within the confined space at this location may play a pathoetiologic role in CRVO. The authors performed radial optic neurotomy in patients with CRVO to relax this space and relieve pressure on the central retinal vein. METHODS: Radial optic neurotomy (RON) was performed on 11 consecutive patients with severe, hemorrhagic CRVO with visual acuities of 20/400 or less. A microvitreoretinal blade was used to relax the scleral ring, cribriform plate, and adjacent sclera of the optic disk. Reperfusion of the retina was achieved via decompressing the central retinal vein. RESULTS: Radial optic neurotomy was performed successfully in all 11 patients. There were no complications noted with this procedure. All patients had clinical improvement as determined by fundus examination, photography, and fluorescein angiography. Postoperative visual acuities were equal or improved in 82% of patients. Eight of the patients (73%) had rapid improvement of visual acuity with an average gain of five lines of vision. CONCLUSIONS: Surgical decompression of CRVO via RON is a technically feasible and initially safe procedure that is associated with rapid reperfusion of the retina. Resolution of the intraretinal hemorrhage, edema, and ischemia may improve the visual prognosis in patients with this common retinal disorder.

Adult↗
PubMed1999

Surgical decompression of branch retinal vein occlusion via arteriovenous crossing sheathotomy: a prospective review of 15 cases.

BACKGROUND: Branch retinal vein occlusion (BRVO), the second most common vascular disorder of the retina, typically occurs at arteriovenous (A/V) crossings where the arteriole and venule share a common adventitial sheath. Mechanical narrowing of the venous lumen at these intersections is thought to play a pathoetiologic role in BRVO. METHODS: We performed surgical decompression of BRVO via A/V crossing sheathotomy in 15 patients with decreased visual acuity due to macular hemorrhage, edema, and ischemia. Reperfusion of the retina was achieved by surgically separating the overlying retinal arteriole from the venule via vitrectomy and adventitial sheathotomy techniques. RESULTS: Intraoperative decompression of the A/V crossing was achieved in all 15 patients. All patients showed clinical improvement as determined by fundus examination, photography, and fluorescein angiography. Postoperative visual acuities were equal or improved in 80% of patients. Ten of the 15 subjects (67%) had improved visual acuity with an average gain of four lines of vision. CONCLUSION: Surgical decompression of BRVO via A/V crossing sheathotomy is a technically feasible procedure that can result in rapid reperfusion of the retina. Resolution of macular hemorrhage, edema, and ischemia may improve visual prognosis in patients with this common retinal vascular disorder.

Aged↗
PubMed1994

Ocular toxoplasmosis misdiagnosed as cytomegalovirus retinopathy in immunocompromised patients.

BACKGROUND: Cytomegalovirus (CMV) and Toxoplasma gondii both cause necrotizing retinopathy in immunosuppressed hosts. Because of the high prevalence of serum antibodies to these agents in the general population and the risks associated with retinal biopsies, diagnosis of these infections is usually based on clinical findings alone, but the two infections can be confused with one another because of similar clinical features. Accurate diagnosis is critical, however, because both diseases are treatable but require different medical therapies. METHODS: Case histories were reviewed for five immunosuppressed patients with necrotizing retinopathy, which was initially diagnosed incorrectly as CMV retinopathy but was subsequently found to be toxoplasmic retinochoroiditis. Correct diagnosis was based on retinal biopsy (2 cases) or rapid response to antiparasitic drug therapy (3 cases). Factors were sought that might help differentiate toxoplasmic retinochoroiditis from CMV retinopathy at presentation. RESULTS: In all cases, the character of retinal opacification (densely opaque, thick) and the appearance of lesion borders (smooth, nongranular) was different from that typically seen with CMV retinopathy. These cases also were characterized by prominent anterior chamber and vitreous inflammatory reactions (four of five cases) and relative lack of retinal hemorrhage. One patient subsequently developed CMV retinopathy; characteristics of the two lesions in the same eye highlighted the differences between these two infections. CONCLUSION: Clinicians should consider ocular toxoplasmosis as a cause of necrotizing retinopathy in immunosuppressed patients and consider an empiric course of antiparasitic therapy for lesions with features described in this report.

Adult↗
PubMed1992

Trimethoprim-sulfamethoxazole therapy for ocular toxoplasmosis.

BACKGROUND: Toxoplasmosis is a leading cause of retinochoroiditis. Conventional multidrug therapy using sulfadiazine, pyrimethamine, and folinic acid is increasingly difficult to procure and administer safely. METHODS: To evaluate the efficacy of trimethoprim-sulfamethoxazole, a fixed-combination antibiotic, patients with active toxoplasmosis were treated with trimethoprim-sulfamethoxazole (Bactrim DS) with or without adjunctive clindamycin and prednisone for 4 to 6 weeks. RESULTS: All patients in this study (n = 16) had resolution of active retinochoroiditis and had improved vision, with an average gain of 5.2 lines of vision. Two patients developed a drug allergy. CONCLUSION: Trimethoprim-sulfamethoxazole appears to be a safe and effective substitute for sulfadiazine, pyrimethamine, and folinic acid (Leucovorin) in treating ocular toxoplasmosis.

Adolescent↗
PubMed1992

Immunohistopathologic findings in herpes simplex virus chorioretinitis in the von Szily model.

After anterior chamber inoculation of herpes simplex virus type 1 (HSV-1), some mice have a characteristic pattern of ocular disease, including ipsilateral anterior uveitis, relative sparing of the ipsilateral retina, and necrotizing contralateral chorioretinitis. It was reported previously that susceptibility to the contralateral chorioretinitis is associated with the Igh-1 locus; congenic mice differing at this locus have different rates of contralateral disease. The immunohistopathologic findings of this model in Igh-1 disparate congenic mice are reported after examining immune cell populations (CD4, CD8, Thy 1.2, Ia, Mac, and immunoglobulin G cells) in both ipsilateral and contralateral eyes and the recruitment kinetics of these cell types in various ocular tissues. In both HSV-susceptible BALB/c and HSV-resistant C.B-17 mice, the ipsilateral eye undergoes early cellular infiltration, and the contralateral retina is devoid of cells until day 10 postinoculation. In BALB/c mice, a late dramatic rise develops in Mac and Ia cells in the ipsilateral and contralateral choroid (P less than 0.005) compared with C.B-17 mice. The C.B-17 mice have an earlier, mild cellular infiltration of the uveal tract in the ipsilateral eye, abrogation of the late Mac and Ia cellular recruitment in the ipsilateral choroid, and an absent contralateral response. These strain-specific immunohistopathologic differences help to explain Igh-1-linked HSV retinitis patterns in this model.

Animals↗
PubMed1991

Limiting dilution analysis of human, tetanus-reactive helper T lymphocytes. A rapid method for the enumeration of helper T lymphocytes with specificity for soluble antigens.

The number of helper T lymphocytes (HTL) in human peripheral blood with specificity for the soluble protein, tetanus toxoid, was estimated by limiting dilution analysis (LDA). HTL were detected via antigen-induced interleukin-2 (IL-2) production, as measured by incorporation of tritiated thymidine by an IL-2-dependent indicator cell line, CTLL-20. Culture conditions optimizing assay sensitivity are described, and the ability to detect antigen-specific HTL using this LDA technique are demonstrated. Observed HTL frequencies in healthy human donors tested for tetanus-reactive helper T cells ranged from less than 1 HTL/268,749 peripheral blood mononuclear cells (PBMC) (undetectable) to 1 HTL/1486 PBMC. The LDA technique was also used to detect frequency shifts in human peripheral blood HTL following challenge with antigen. This assay offers distinct advantages over proliferative LDA techniques in that it is rapid (requiring only 2 days), and defines an antigen-reactive T cell subset with defined function (IL-2 secretion). Furthermore, the LDA technique can be adapted for the detection of other soluble protein antigens, such as PPD and Candida albicans. In general, this LDA technique provides a reliable, quantitative index of human HTL reactivity to any of a variety of soluble protein antigens, and has clinical as well as experimental applicability.

Animals↗
PubMed1991

Enumeration of autoreactive helper T lymphocytes in uveitis.

In a one-stage, interleukin-2 (IL-2), limiting-dilution analysis, peripheral blood mononuclear cells from patients with uveitis and normal control subjects were assayed for S-antigen specific, tetanus-specific, and in vivo activated helper T cells. Controls subjects consistently demonstrated tetanus-specific responses, but neither in vivo activation nor S-antigen specific helper T cell responses were seen. Patients with active forms of diffuse, posterior, and anterior uveitis were found to have significant frequencies of both in vivo activated and S-antigen specific helper T cells in their peripheral blood. These data show that patients with certain forms of uveitis have a measurable frequency of lymphocytes in the peripheral immunologic compartment capable of secreting IL-2 in response to autologous presentation of ocular autoantigen (S-antigen). Limiting-dilution analysis techniques, generating minimal responder cell frequency estimates and distinct IL secretion patterns, may provide an index of disease activity and critical information about the mechanism(s) of ocular inflammation.

Antigens↗
PubMed1990

Histology and immunohistology of Igh-1-restricted herpes simplex keratitis in BALB/c congenic mice.

In order to characterize the local ocular immunologic milieu of Igh-1-restricted herpes simplex keratitis (HSK), we investigated histologic and immunohistologic correlates of disease over a 21-day time course. Clinically observable keratitis began 10 days postinoculation in susceptible C.AL-20 (Igh-1d) and moderately susceptible BALB/c (Igh-1a) mice, whereas HSV-1-resistant C.B-17 (Igh-1b) mice rarely developed disease. Igh-1-restricted histologic differences were observed by day 11 postinoculation; C.AL-20 and BALB/c mice showed augmented recruitment of neutrophils and mononuclear cells in conjunctival, limbal, and corneal tissues compared to C.B-17 mice. On immunohistologic study, Lyt-1 to Lyt-2 cell ratios by day 11 postinoculation were 7:1, 2:1, and 1:8 in corneas from C.AL-20, BALB/c, and C.B-17 mice, respectively. Macrophages and neutrophils were absent in corneas from C.B-17 mice at this time, but could be found in large numbers in the corneas of susceptible mouse strains through day 21. These data demonstrate a strong relationship between Igh-1 phenotype and inflammatory cell recruitment in response to corneal infection with HSV-1, and support a role for T cell subpopulations in mediating Igh-1-restricted HSK.

Animals↗
PubMed1990

Viral isolation and systemic immune responses after intracameral inoculation of herpes simplex virus type 1 in Igh-1-disparate congenic murine strains.

Igh-1-disparate congenic murine strains differ in their susceptibility to develop contralateral chorioretinitis after intracameral (AC) inoculation with Herpes simplex virus type 1 (HSV-1): 75% of BALB/cByJ (Igh-1a) and 5% of C.B-17 (Igh-1b) develop necrotizing chorioretinitis. To determine the mechanism of influence of host genetics on development of contralateral chorioretinitis, the authors did viral isolation studies in contralateral eyes, determined in vivo and in vitro T-cell responses, and HSV-antibody levels at various times after AC inoculation of BALB/cByJ and C.B-17 mice with HSV-1. Viral isolation was similar in both mouse strains (P less than 0.2). Similarities in systemic immune responses included suppressed delayed-type hypersensitivity responses 5 days, cytotoxic T-lymphocyte and lymphocyte proliferation responses 8 days, and viral neutralizing antibody titers 5 days postinoculation (PI). Differences in systemic immune responses included: (1) delayed-type hypersensitivity responses were not suppressed in C.B-17 mice (P greater than 0.1) and were hyperactive in BALB/cByJ mice (P less than 0.025) 10 days PI and (2) HSV-neutralizing antibody production was higher in C.B-17 mice 10 days PI. These data suggest that the mere presence of HSV-1 in the uninoculated eye is insufficient for the development of chorioretinitis. Virus-specific delayed-type hypersensitivity reactions might be involved in the pathogenesis of retinitis in BALB/cByJ mice; and virus-neutralizing antibodies and suppressed HSV-specific delayed-type hypersensitivity reactions might be instrumental in the protection enjoyed by C.B-17 mice.

Animals↗
PubMed1989

Evidence for the potential influence of cyclic nucleotides on maintenance of or reactivation from latency of herpes simplex virus in trigeminal ganglionic neurons.

Herpes simplex virus infections are epidemic throughout developed countries, and recurrent herpes simplex keratitis is the most common cause of corneal blindness in these countries, NIH (1973). No available antiviral agent is capable of eradicating the state of viral ganglionic latency, and hence no effective treatment currently exists for prevention of viral re-activation from latency, with resultant recurrent infectious viral clinical manifestations. Putative triggers of re-activation include stress, sunburn, menses, trauma, and fever. These 'triggers' seem to share at least one common characteristic: the potential ability to influence intracellular cyclic nucleotide levels through the action of such first order messengers as catacolamines (stress, trauma) and/or arachadonic acid metabolites (sunburn, fever, trauma, and menses). We exploited an in vitro model of HSV ganglionic latency, and developed a model of in vitro organ culture ganglionic viral reactivation from latency. We then examined the effect of a variety of agents on this model. We found that agents which have been shown to elevate cyclic AMP levels consistently produce increased viral shedding (compared to control, spontaneous reactivation rate) in our model of viral reactivation from latency. In contrast, agents which have been shown to depress c-AMP levels and/or to elevate c-GMP levels inhibit viral reactivation from latency in this in vitro model. We conclude that intracellular cyclic nucleotide levels may influence events which control herpes simplex genome transcription.

Animals↗
PubMed1989

In vitro demonstration of human natural killing of keratocytes and corneal epithelium.

Cultured human corneal keratocytes or fresh human lamellar corneal epithelial sections were used as target cells in a monolayer cytotoxicity assay. Fresh allogeneic nonadherent peripheral blood mononuclear cells were incubated with the corneal-cell populations and assayed for lymphocyte binding and target-cell cytotoxicity by acid-violet-49 vital staining. Primary keratocyte populations bound lymphocytes, and there was subsequent keratocyte dye uptake. Corneal epithelium did not show either binding or lymphocyte-mediated cytolysis. These data suggest that nonspecific and spontaneous lymphocyte-mediated cytolysis of keratocytes occurs in vitro and that the responsible lymphocyte subpopulation has functional activities and cellular morphology characteristic of the natural-killer cell. This activity may play a role in initiating specific corneal-graft rejection.

Cytotoxicity, Immunologic↗
PubMed1989

Chorioretinal disease patterns in congenic mice following intraocular inoculation with HSV-1.

Disease patterns and immunologic parameters were studied employing inbred and Igh-1 disparate congenic mice to determine the role of host genetics and Igh-1-linked gene products in the von Szily model of viral chorioretinitis. Following intracameral inoculation of 1.5 x 10(4) PFU HSV-1 (KOS), 100% of BALB/c (Igh-1a), 62% of A/J (Igh-1e) and none of the C57BL/6J (Igh-1b) inbred mice developed contralateral necrotizing chorioretinitis. Multigenic differences between inbred mice prohibit conclusions about the specific role of Igh-1-linked immune regulation in this model. In order to more exactly define Igh-1-specific restriction of HSV-1-mediated chorioretinitis, Igh-1-disparate, congenic BALB/c mice were studied following both anterior chamber and intravitreal inoculation protocols. Anterior chamber inoculation resulted in contralateral retinal necrosis in 75% of BALB/c (Igh-1a) mice, 30% of C.AL-20 (Igh-1d) and 5% of the C.B-17 (Igh-1b) congenic mice; all strains showed ipsilateral retinal sparing. Following intravitreal inoculation of HSV-1 a similar restricted disease pattern was found in contralateral eyes. Contralateral chorioretinitis developed in 30% of BALB/c, 15% of C.AL-20 and 6% of C.B-17 mice. Ipsilateral disease, however, was found in all murine strains. These disease patterns developed despite equivalent suppression of systemic DTH and equivalent RPE permissivity to viral replication. These data demonstrate that host genetics strongly regulates contralateral HSV-1-mediated chorioretinal disease patterns by a mechanism unrelated to the development of systemic suppression of DTH and specifically support a dominant role for gene products linked to the Igh-1 locus in the immunomodulation of ocular disease.

Animals↗
PubMed1989

Herpes simplex virus type-1 strain influence on chorioretinal disease patterns following intracameral inoculation in Igh-1 disparate mice.

We have previously shown that the Igh-1 locus on chromosome 12 of the mouse influences contralateral disease patterns in the modified von-Szily model. Following intracameral injection with 1.5 X 10(4) PFU of HSV strain KOS (HSV-KOS), 75% of BALB/cByJ (Igh-1a), 30% of C.AL-20 (Igh-1d) and 5% of C.B-17 (Igh-1b) mice develop contralateral chorioretinal necrosis. In contrast, Igh-1 congenic mice do not develop contralateral chorioretinal necrosis following anterior chamber inoculation of the same dose of an HSV-KOS mutant lacking surface glycoprotein-C (HSV-GC-KOS). Similarly, injection of wild type HSV strain mP (HSV-mP) into the anterior chamber of susceptible BALB/cByJ mice induces destructive contralateral chorioretinitis whereas injection of the same dose of the mutant HSV strain MP (HSV-MP) lacking surface glycoprotein-C does not induce a destructive contralateral chorioretinitis. In addition, higher doses of HSV-mP inoculum abrogate the Igh-1-associated contralateral chorioretinal protection seen in C.B-17 mice; protection is restored in C.B-17 mice at lower HSV-mP doses that still cause contralateral chorioretinitis in BALB/cByJ mice. These data demonstrate the influence of the viral isolate on the modified von-Szily model and specifically the requirement for the presence of glycoprotein-C on the surface of HSV for the development of contralateral destructive chorioretinitis.

Animals↗
PubMed1988

Immunomodulation of experimental murine herpes simplex keratitis: I. UV-HSV protection.

A/J mice were immunized subcutaneously with ultraviolet light (UV) inactivated herpes simplex virus type-1, MP strain (HSV-MP). Control A/J mice were immunized subcutaneously either with media (unimmunized controls) or with live HSV-MP (immunized controls). Immunized and control mice were challenged ocularly with either MP or mP strain HSV-1 after corneal scarification and were followed for 3 weeks post corneal challenge. The mice were observed during this time period for signs of herpes simplex keratitis (HSK), lid lesions and encephalitis. At the time of sacrifice, the ipsilateral trigeminal ganglia were removed and assayed for latent HSV-1 using cocultivation on Vero cell monolayers. The results of these studies demonstrated that immunization with UV inactivated HSV (UV-HSV) gave the same protection against keratitis and encephalitis as immunization with live virus. Furthermore, the cocultivation assays indicated that immunization with either live HSV-1 or UV inactivated HSV-1 protected against the establishment of latency.

Animals↗
PubMed1988

Immunomodulation of experimental murine herpes simplex keratitis: II. Glycoprotein D protection.

Subcutaneous immunization with purified HSV-1 glycoprotein D (gD) protects susceptible A/J mice against keratitis and encephalitis following corneal HSV-1 challenge. Mice were immunized with gD, in complete Freund's adjuvant, 3.0 micrograms/mouse followed by two booster doses of 1.5 micrograms/mouse at weeks 2 and 4. Control groups of A/J mice were injected with either complete Freund's adjuvant (unimmunized controls) or live HSV-1 MP strain (immunized controls). All mice were challenged ocularly at week 5 with HSV-1, F strain (6.5 x 10(3) PFU) after corneal scarification. None of the 16 animals immunized with gD developed stromal keratitis; only 3 out of 12 animals immunized with live HSV-1 developed a stromal keratitis; 13 out of 16 CFA primed unimmunized mice developed severe stromal keratitis within 14 days post corneal challenge, and 3 out of 16 control CFA primed animals died within 16 days post corneal challenge. At the time of sacrifice (3 weeks post corneal challenge), the ipsilateral trigeminal ganglia were removed and assayed for latent HSV-1 using cocultivation on Vero cell monolayers. The results of these experiments indicate that immunization with gD produces protection against latent ganglionic infection in 56% of the immunized animals, and provides protection against keratitis and death following HSV corneal challenge.

Animals↗
PubMed1988

Ganglionic permissivity to HSV-1 replication and acyclovir-induced latency: an in vitro model.

HSV-1 is known to establish latent infections in murine trigeminal ganglia. In order to study the genetic influence of the host on permissivity to HSV-1 replication and latency in mouse trigeminal ganglia, an in vitro culture system was developed. Ganglia from HSV sensitive A/J and resistant C57BL/6J mice were harvested and inoculated in vitro with either MP or KOS strains of HSV-1. Infected ganglia were placed in culture for 7 days with or without 150 micrograms/ml acyclovir. Ganglia were then homogenized and assayed for infectious particles or frozen whole for standard immunostaining. A/J ganglia without acyclovir consistently demonstrated a three-fold higher viral replication compared to C57BL/6J ganglia without acyclovir for both MP and KOS. Indirect immunofluorescent staining of actively infected ganglia using rabbit anti-HSV antiserum showed increased staining in A/J ganglionic axons compared to C57BL/6J ganglionic axons. Ganglia from both murine strains showed total suppression of viral replication with acyclovir treatment. Immunostaining for latent viral protein with mouse monoclonal anti-ICP-4 (VP 175) was positive for both A/J and C57BL/6J strains following acyclovir treatment. Desuppression of acyclovir-treated whole ganglia resulted in 54% spontaneous HSV reactivation. These results suggest that: (1) HSV-1 can establish an active infection in whole murine trigeminal ganglia in vitro; (2) HSV-1 replicates to a greater extent in A/J ganglia compared to C57BL/6 ganglia; and (3) in vitro HSV-1 ganglionic infection in both murine strains is equally suppressed to a latent state by acyclovir treatment.

Acyclovir↗