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)

Drugs used for the inhibition of DNA viruses, such as iododeoxyuridine, adenine arabinoside, or trifluorothymidine, are not biochemically selective in their action and also interfere with normal cellular functions. The recently reported 9-(2-hydroxyethoxymethyl)guanine (acycloguanosine) is selectively phosphorylated by viral thymidine kinase but not by normal cellular thymidine kinase. Our present studies show that the acycloguanosine is as effective in treating herpetic keratitis in the rabbit as iododeoxyuridine and trifluorothymidine when given topically as an ointment. It is also effective when given intravenously for the treatment of herpetic iritis and is effective in preventing death from encephalitis in rabbits.
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PMID:Effect of 9-(2-hydroxyethoxymethyl)guanine on herpesvirus-induced keratitis and iritis in rabbits. 21 1

Previous results obtained in experimental and clinical trials have demonstrated that topical combined thrapy with human interferon (HI) and human colostral secretory immunoglobulin A (S-IgA) is effective against herpetic corneal infection. This therapy prevented encephalitis in rabbits but could not completely prevent recurrences either in rabbits or in patients. A number of in vitro studies were designed to elucidate the role of these factors in herpes simplex virus replication in the nervous system, with the following results: (1) HSV latency in trigeminal ganglia (TG) explanted from rabbits with experimental herpetic keratitis, topically treated with HI or HI/S-IgA: HSV was recovered in 30% TG after 15-19 days co-cultivation on RK-13 cells. (2) HSV replication in nervous ganglia and nerve of newborn rabbits in organ culture; influence of HI or HI plus IgG: a restrictive HSV productive infection was demonstrated in this system, although yields were always higher in nerve cultures. We were unable to demonstrate a direct effect of HI on HSV-1 replication. When explants were treated with HI and IgG before and after infection for 48 hours a delay in the expression of HSV-1 was detected by co-cultivation. (3) Replication of HSV-1 and HSV-2 in a C1300 murine neuroblastoma clone (NB41A3): both HSV types replicated with titres of 10(3.4) for HSV-1 AND 10(4.8) for HSV-2 at 48 hours p.i.; CPE was more marked for HSV-2 at 24 hours. HSV-specific antigens were demonstrated by the immunoperoxidase technique.
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PMID:Interferon in the replication of herpes simplex virus in normal and pathological nerve cells. 22 73

The history of herpetic keratitis is presented. The similarities and differences between dendritic keratitis and herpes labialis are enumerated, with the suggestion that the similarities (in onset, pathology, and clinical course) far outweigh the differences. The principal difference seems to be that the avascalarity of the cornea retards the immunologic responses. Important points in the history of herpetic keratitis include (1) the close association of herpetic disease with malaria around the turn of the century; (2) the relatively benign nature of the disease, in contrast to herpes zoster keratitis; (3) the unfavorable response of the disease to immunosuppressive measures and diseases; (4) the failure of chemotherapy to influence favorably the natural history of the disease; and (5) the increasing visual damage caused by the disease since 1952 when corticosteroids were introduced into ocular therapy. Mention is made of the increasing problem of venereal herpes, with resultant neonatal herpetic keratitis, retinitis, and encephalitis.
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PMID:Historical observations on herpetic keratitis. 79 Jun 18

Athymic (nude) mice have played an important role in defining the function of the immune system and its role in infectious diseases. In the majority of these studies, heterozygous +/nu mice have been used as normal controls for the nu/nu mice, and it has been assumed that +/nu mice have essentially normal immune systems. We have compared the response of +/+, +/nu and nu/nu BALB/c mice following ocular infection with HSV-1 and have found that +/nu mice develop significantly more severe blepharitis, vascularization of the cornea, stromal keratitis and extraocular disease (herpetiform spread) than +/+ BALB/c mice. The extraocular disease was particularly severe in the +/nu mice, suggesting that factors regulating herpetiform spread of the virus are deficient in these mice. Susceptibility to lethal encephalitis did not differ between +/+ and +/nu mice. These results suggest that significant differences exist in the response to ocular HSV infection between +/+ and +/nu mice.
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PMID:Susceptibility of +/+, +/nu and nu/nu BALB/c mice to ocular herpes simplex virus infection. 128 12

Passive administration of antibody against herpes simplex virus type 1 (HSV-1) has been shown to protect against stromal keratitis and death from encephalitis. Although the exact mechanism by which passively-transferred antibody protects is not known, one of the features of protection by passively-transferred antibody is interference with the ability of the virus to spread within the nervous system. In the experiments reported herein, studies were performed to determine if 8D2, a monoclonal antibody against a type-common epitope of glycoprotein D, could protect mice from retinal necrosis following uniocular anterior chamber inoculation of HSV-1. Mice were protected from retinal necrosis when the antibody was administered 2 hours before virus inoculation or 24 hours after virus inoculation. When antibody was injected 2 hours before virus inoculation, the titer of virus at day 1 p.i. in the injected eyes of antibody-treated and control mice was the same, but by 3 days p.i., the titer of virus in the antibody-treated mice was significantly lower than that recovered from control mice. The titers of virus in the brains and in the uninoculated eyes of antibody-treated mice were also significantly lower than in control mice. The results of these studies suggest that passively-transferred antibody protects against retinal necrosis by limiting spread of virus to the CNS or replication of virus within the CNS.
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PMID:Protection from retinal necrosis by passive transfer of monoclonal antibody specific for herpes simplex virus glycoprotein D. 131 51

Measles encephalitis was produced in 41 hamsters by intracerebral injection of the hamster-neuroadapted Mantooth HBS viral strain. Group I (n = 10) included 2-day old (newborn) hamsters, each inoculated with 0.02 ml of 1:20 diluted virus. This group was sacrificed 4 days postinoculation (DPI). Group II (n = 31) included 25-day old hamsters, each inoculated with 0.03 ml of 1:10 diluted virus. This group was sacrificed 6, 13, 17, and 31 DPI. Clinical and histological evidence of measles encephalitis was present in all infected hamsters. Retinal lesions varied with the age of the animals at the time of inoculation. Retinal folds were observed in the 2-day old group and represented one form of retinal dysplasia. In the 25-day old group, however, earliest retinal involvement was in the form of hemorrhages, followed by focal retinitis in animals sacrificed 6-17 DPI. Measles keratitis was noted only in animals sacrificed 6 DPI. In 25-day old hamsters, measles keratitis and retinal hemorrhages represented the acute manifestations, whereas retinitis occurred later. However, ocular involvement did not correlate with the degree of severity of measles encephalitis.
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PMID:Eye pathology associated with measles encephalitis in hamsters. 187 85

Passive transfer of a monoclonal antibody (MAb) specific for glycoprotein D (gD) is highly effective in preventing the development of herpes simplex virus type 1-induced stromal keratitis. In the present study, we investigated whether animals which had been functionally depleted of T-cell subsets or asialo GM1+ cells would continue to be responsive to MAb therapy. BALB/c mice were depleted of CD4+, CD8+, or asialo GM1+ cells by treatment with anti-L3T4, anti-Lyt 2.2, or anti-asialo GM1 antibodies, respectively. Functional depletion of CD4+ cells was documented by the loss of delayed-type hypersensitivity responsiveness, while CD8+ cell depletion was accompanied by abrogation of cytotoxic lymphocyte activity. Anti-asialo GM1 treatment led to the loss of natural killer cell lytic activity. Mice depleted of the desired cell population and infected on the scarified cornea with herpes simplex virus type 1 uniformly developed necrotizing stromal keratitis by 3 weeks postinfection. A single inoculation of anti-gD MAb (55 micrograms) given intraperitoneally 24 h postinfection strongly protected hosts depleted of CD4+ cells against stromal keratitis. Likewise, antibody treatment in CD8+ or asialo GM1+ cell-depleted hosts was as therapeutically effective as that seen in non-cell-depleted mice. We also observed that in cell-depleted mice, the virus spread into the central nervous system and caused encephalitis. The CD4+ cell-depleted mice were the most severely affected, as 100% developed fatal disease. Anti-gD MAb treatment successfully protected all (32 of 32) CD4+-, CD8+-, or asialo GM1(+)-depleted hosts against encephalitis. We therefore conclude that antibody-mediated prevention of stromal keratitis and encephalitis does not require the obligatory participation of CD4+, CD8+, or asialo GM1+ cells. However, when mice were simultaneously depleted of both CD4+ and CD8+ T-cell subsets, antibody treatment could not prevent fatal encephalitis. Thus, antibody can compensate for the functional loss of one but not two T-lymphocyte subpopulations.
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PMID:Anti-glycoprotein D monoclonal antibody protects against herpes simplex virus type 1-induced diseases in mice functionally depleted of selected T-cell subsets or asialo GM1+ cells. 192 Jun 24

Free-living amoebae causes three well-defined disease entities: (i) primary amoebic meningoencephalitis, caused by Naegleria fowleri, (ii) granulomatous amoebic encephalitis and (iii) chronic amoebic keratitis, caused by species of Acanthamoeba. Both Naegleria infections and chronic amoebic keratitis occur in healthy individuals while granulomatous amoebic encephalitis is often associated with patients with acquired immunodeficiencies. The different pathogenic behaviour of these organisms is associated with differences in life cycle, amoeboidal locomotion, enzyme composition (such as phospholipase A), and cytotoxins, as well as natural host immunity. Immunity against these amoebae (whether acquired or natural) involves a combination of complement, antibody and cell-mediated immunity. Evidence suggests that the major mechanisms of immunity against these amoebae is activation of phagocytic cells, especially neutrophils, by lymphokines and opsonization of the amoebae by antibody which promote an antibody dependent cellular destruction of the organism.
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PMID:Free-living amoebae: pathogenicity and immunity. 201 36

Infections caused by small, free-living amebas are still unfamiliar to many clinicians, pathologists, and laboratorians. As of 31 July 1989, more than 140 cases of primary amebic meningoencephalitis caused by Naegleria fowleri and more than 40 cases of granulomatous amebic encephalitis caused by Acanthamoeba species (including two cases in patients with AIDS) and possibly by other free-living amebas had occurred worldwide. The recent increase in acanthamoeba keratitis (more than 200 cases), especially in contact lens wearers, has generated new interest in this group of amebas. Effective treatment is still lacking. Risk factors, clinical manifestations, and laboratory parameters helpful in the recognition of infections of the central nervous system (i.e., granulomatous amebic encephalitis and primary amebic meningoencephalitis) and acanthamoeba keratitis are reviewed.
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PMID:Naegleria and Acanthamoeba infections: review. 219 54

To identify causes of mortality in young captive crocodiles, detailed necropsy and laboratory examination was done on 54 (30 Crocodylus porosus, 22 C. novaeguineae, 2 of unrecorded species). Although multiple infections often confounded interpretation it was concluded that the major infectious diseases, of approximately equal importance, were coccidiosis, bacterial septicaemia with Gram-negative organisms, and metazoan parasitism including ascariasis and pentastomiasis. A range of other lesions and agents was recognised, including keratitis, enteritis of unknown aetiology, non-suppurative encephalitis, traumatic peritonitis and trematodes located in renal tubules, gut and blood vessels. Some crocodiles in poor condition had only mild lesions associated with metazoan parasites and the cause of death or illness could not be clearly determined, although it was considered likely that adaptation failure was a contributing factor.
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PMID:Diseases of young captive crocodiles in Papua New Guinea. 226 4


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