Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 63-year-old man, who had for one month been on sulfasalazine therapy, developed general malaise, high fever, severe stomatitis, and bilateral necrotizing pseudomembranous conjunctivitis with corneal erosion, identical to that seen in the Stevens-Johnson syndrome. Topical therapy with antibiotics and aprotinin rapidly healed the corneal surfaces, while densely adherent true membranes developed on the conjunctiva, and were removed surgically several times during the next week. After the acute stage, subtle subepithelial conjunctival scarring, superficial punctate keratitis, dry eye syndrome and fluctuating irregular corneal astigmatism became evident, but good visual acuity, lid function and ocular motility were retained. Histopathologic study of conjunctival membranes from two cases of membranous conjunctivitis revealed polymorphonuclear leukocytes within a matrix composed of fibrin, tenascin and fibronectin. In older membranes, histiocytes were additionally found. Surgical debridement of such membranes removes a substratum of inflammatory debris that is likely to promote secondary infection, fibrosis and symblepharon formation, and may decrease rather than increase subsequent scarring of the necrotized conjunctiva.
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PMID:Pseudomembranous and membranous conjunctivitis. Immunohistochemical features. 138 71

Swine, a natural host species for infection by vesicular stomatitis virus (VSV), were infected with VSV-New Jersey (VSV-NJ) serotype virus obtained from a recent field isolate. Tissues collected from the infected pigs were examined for the presence of infective virus, for viral antigens, and/or for viral nucleic acid. Infective virus could be recovered from tissues near the site of infection for as long as 6 days after the primary infection with VSV. However, no infective virus was recovered following hypothermia induced 11 weeks after infection, or following a secondary challenge with virus 22 weeks after initial infection. Immunofluorescence tests for viral antigens and nucleic acid hybridization assays failed to detect viral antigens or nucleic acids in tissues from which no infective virus could be recovered. Titers of serum-neutralizing antibody peaked 3-5 weeks after infection and then fell slightly until the secondary infection which caused a rapid anamnestic response. Peripheral blood mononuclear cells (PBM) tested 3, 5, 8 or 18 weeks after primary infection all produced readily detectable antigen-specific proliferative responses when cultured with VSV. Thus, although direct tests failed to demonstrate persistence of virus after infection, the humoral and cellular immune response remained elevated for months. Infective VSV was not required to stimulate the proliferative response since UV-inactivated VSV was immunogenic in these in vitro tests. Following primary infection, antigen-specific proliferative responses could be stimulated by several strains of VSV-NJ, but not by VSV-Indiana (VSV-Ind) serotype virus. Secondary infection had relatively little effect on the proliferative response to VSV-NJ strains, but it did cause the PBM to gain responsiveness to VSV-Ind.
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PMID:Experimental vesicular stomatitis virus infection of swine: extent of infection and immunological response. 247 Jan 90

Previously, we demonstrated that memory cell-mediated immune responses can be generated in Pichinde virus (PV)-primed mice after secondary challenge in vivo with homologous virus. Further, treatment of mice with cyclophosphamide (CY) before primary infection with PV abrogated the generation of H-2-restricted, virus-specific cytotoxic T lymphocytes (CTL), and rechallenge of these mice was followed by neither a primary nor a secondary CTL response. Here, we demonstrate that this CY-induced block in memory anti-PV CTL generation was not due to establishment of a persistent infection. Interestingly, this CY-induced block in memory anti-PV CTL generation was overcome by secondarily coinfecting mice with PV and lymphocytic choriomeningitis virus (LCMV) or PV and Tacaribe virus. Secondary infection with LCMV or Tacaribe virus alone did not elicit anti-PV CTL. Coinfection resulted in the generation of a PV-specific memory CTL response as judged by maximal activity on day 4 after rechallenge. Co-infection with PV and vesicular stomatitis virus, an unrelated rhabdovirus, did not efficiently restore memory anti-PV CTL responses. Memory anti-PV CTL responses were also restored when interleukin 2 (IL 2)-containing supernatants were injected i.p. after rechallenge of CY-treated mice with PV. To demonstrate that IL 2 was the responsible lymphokine in these preparations, highly purified IL 2 was added to in vitro cultures of spleen cells from CY-treated PV-primed mice. In the presence of PV-infected syngeneic macrophages, addition of purified IL 2 resulted in a dose-dependent restoration of H-2-restricted anti-PV CTL activity. The CTL precursor (CTLp) frequency of CY-treated PV-primed mice was markedly decreased from that of normal PV-primed mice. Thus, the long-lasting block in the ability to generate a PV-specific memory CTL response after CY treatment appears to be due to both a lack of helper T cell activity and a significant reduction of CTLp. However, this block may be overcome by coinfecting with viruses that cross-react at the helper T cell level or by exogenous treatment with highly purified IL 2.
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PMID:Abrogation of anti-Pichinde virus cytotoxic T cell memory by cyclophosphamide and restoration by coinfection or interleukin 2. 298 65

Dental practitioners should be familiar with Darier's disease because oral lesions of the disease may resemble other diseases. Differential diagnosis should include papillary hyperplasia of the palate, acanthosis nigricans, Cowden's disease, nicotine stomatitis, and condyloma acuminatum. Careful observation of the oral and skin lesions and consideration of the medical and family history should assist in diagnosis. Vitamin A, given in high doses, has been used with variable success in the treatment of Darier's disease. Systemic corticosteroids have been used with good results, but these require prolonged use as they are not curative. Secondary infection is a common complication for which topical corticosteroids are helpful.
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PMID:Irregular papular lesions of the hard palate. 693 Nov 67

Mucocutaneous side effects of chemotherapeutic agents are frequent, especially alopecia and stomatitis. The latter can be dose limiting or can endanger the patient in case of secondary infection. Nail changes and hyperpigmentation are cosmetically disturbing. For the diagnosis of the acral erythrodysesthesia syndrome and the neutrophilic eccrine hidradenitis knowledge of the clinical presentation is required. Interaction of chemotherapeutic agents with radiotherapy or UV light can aggravate or cause skin changes like the radiation recall. Despite the completely different mode of action of new substances or immunotherapeutic agents like monoclonal antibodies the same range of side effects can be observed.
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PMID:[Adverse chemotherapy effects on skin and mucous membranes]. 1210 57

Intracellular pathogens are capable of inducing vigorous CD8+ T cell responses. However, we do not entirely understand the factors driving the generation of large pools of highly protective memory CD8+ T cells. Here, we studied the generation of endogenous ovalbumin-specific memory CD8+ T cells following infection with recombinant vesicular stomatitis virus (VSV) and Listeria monocytogenes (LM). VSV infection resulted in the generation of a large ovalbumin-specific memory CD8+ T cell population, which provided minimal protective immunity that waned with time. In contrast, the CD8+ T cell population of LM-ova provided protective immunity and remained stable with time. Agonistic CD40 stimulation during CD8+ T cell priming in response to VSV infection enabled the resultant memory CD8+ T cell population to provide strong protective immunity against secondary infection. Enhanced protective immunity by agonistic anti-CD40 was dependent on CD70. Agonistic anti-CD40 not only enhanced the size of the resultant memory CD8+ T cell population, but enhanced their polyfunctionality and sensitivity to antigen. Our data suggest that immunomodulation of CD40 signaling may be a key adjuvant to enhance CD8+ T cell response during development of VSV vaccine strategies.
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PMID:Agonistic anti-CD40 enhances the CD8+ T cell response during vesicular stomatitis virus infection. 2516 94