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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a detailed study on oral lesions and their association with the WHO revised provisional case definition of AIDS as well as serologic signs of HIV infection among 186 patients in Dar Es Salaam, Tanzania. The patient material consisted of 39 hospitalized suspected AIDS patients, 44 medical nonsuspected patients, 53 dental outpatients, and 50 patients with sexually transmitted diseases. The male:female ratio was 2.1:1 on average. Oral examination was done without knowledge of the HIV status of the patients. Among 39 suspected AIDS patients 97% had WHO AIDS criteria and 90% were seropositive for HIV. Among the 147 patients not suspected of having AIDS 18 (12%) had AIDS criteria and 15% had serologic evidence of HIV infection. The presence of WHO AIDS criteria correlated significantly with the presence of HIV antibodies, but not with HIV antigen. Oral lesions were found in 54% of those with AIDS criteria and 52% of HIV-infected patients, as compared to 3% and 6% of the patients without AIDS criteria and HIV infection, respectively (p less than 0.01). Among patients with AIDS atrophic candidiasis occurred in 21%, pseudomembranous candidiasis in 23%, hairy leukoplakia in 36%, herpetic stomatitis in 2%, Kaposi's sarcoma in 4%, and nonspecific ulcer in 4%. The presence of oral lesions had a high predictive value for presence of AIDS criteria as well as for presence of HIV infection in this hospital setting. All patients should have a thorough oral examination and the presence of the aforementioned oral lesions should lead to testing for HIV infection.
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PMID:Oral candidiasis and hairy leukoplakia correlate with HIV infection in Tanzania. 218 50

This report describes a case of HIV-associated periodontitis complicated by necrotizing stomatitis in a homosexual male patient with AIDS. Necrotizing stomatitis is a rapidly progressive ulcerative and necrotic infection that causes massive destruction of the oral tissues and underlying bone. Like HIV periodontitis, it appears to be related to the immune suppression caused by human immunodeficiency virus (HIV) infection; importantly, it may be life threatening. In this case, initial resolution resulted from local debridement in association with metronidazole therapy. Long-term clinical management consisted of monthly professional prophylaxis, good oral hygiene, and daily rinses with chlorhexidine. This case suggests that progressive oral necrotizing infection should be recognized as one element in the spectrum of oral manifestations of HIV infection.
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PMID:HIV-associated periodontitis complicated by necrotizing stomatitis. 231 60

From January 1988-September 1989, dental practitioners performed a comprehensive oral examination on 83 HIV positive patients at the Department of Infectious Diseases, University Clinic of Internal Medicine in Kinshasa, Zaire for a study on prevalence and clinical aspects of oral lesions associated with HIV infection. Women comprised 55.5% of these AIDS patients. They all had oral lesions: 94% fungal, 33% bacterial, 23% viral, 14% unknown origin, and 12% neoplasms. The majority of these oral lesions developed in 31-40 year olds. Further, the 21-30 year olds were more likely to have bacterial infections, especially aggressive periodontitis. Fungal infections occurred most often on the lips, palate, and tongue, while viral infections occurred mainly on the tongue. Kaposi's sarcoma only afflicted the palate. Pseudomembranous candidiasis was the leading fungal infection (32% of all oral lesions) then atrophic (22.8%) and hyperplastic (6%) types. 17% and 16% of all lesions included these bacterial infections: aggressive periodontitis and necrotizing gingivitis respectively. the leading viral infection was hairy leukoplakia (14%) followed by leukoplakia (8%), and herpetic stomatitis (4%). The unknown lesions included ulcers (12%) and a swollen salivary gland )2%). 12% of the examined AIDS patients, mostly 31-50 year olds, had oral Kaposi's sarcoma. They also had it on other parts of the body. Since HIV prevalence in Zaire ranges between 3-8%, all dentists should be cognizant of oral manifestations of HIV which may indeed be the 1st clinical indications of HIV. They should refer any patients with such lesions to a health facility with AIDS specialists for diagnosis and care.
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PMID:Oral manifestations of AIDS in a heterosexual population in a Zaire hospital. 235 42

The production of neutralizing monoclonal antibodies (MAbs) will permit the exact localization of neutralizing epitopes on the AIDS virus, HIV-1. We describe the properties of seven MAbs to the envelope of the LAV-1 isolate. Five MAbs recognise the central portion of gp110, amino acids 279-472, and four of these are capable of high-titre neutralization of HIV-1, by infection inhibition, syncytial inhibition and vesicular stomatitis virus (VSV) pseudotype neutralization. One of the two MAbs to gp41 inhibits syncytium formation. Neutralization, live cell immunofluorescence and immunoprecipitation of gp110 are type-specific and restricted to HIV-1 isolates closely related to LAV-1.
AIDS 1988 Feb
PMID:Neutralizing monoclonal antibodies to the AIDS virus. 245 22

Mannan sulfate, a novel sulfated polysaccharide, was prepared and investigated for its activity against human immunodeficiency virus type 1 (HIV-1) in vitro. Mannan sulfate completely inhibited HIV-1-induced cell destruction and viral antigen expression in HIV-1-infected Molt-4 (clone 8) cells at a concentration of 4 micrograms/ml. The 50% antiviral effective doses obtained with mannan sulfate in Molt-4 (clone 8) cells and in MT-4 cells were 1.5 and 9.3 micrograms/ml, respectively. No toxicity for Molt-4 (clone 8) cells or MT-4 cells was observed at a concentration of 4,000 and 2,500 micrograms/ml, respectively. Mannan sulfate was also inhibitory to other enveloped viruses, i.e. herpes simplex virus types 1 and 2, vaccinia virus and vesicular stomatitis virus. These results suggest that mannan sulfate may be useful for the chemotherapy of various viral infections, including those causing and associated with AIDS.
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PMID:In vitro activity of mannan sulfate, a novel sulfated polysaccharide, against human immunodeficiency virus type 1 and other enveloped viruses. 256 84

We describe the identification, experimental transmission, and pathogenesis of a naturally occurring powerfully immunosuppressive isolate of feline leukemia virus (designated here as FeLV-FAIDS) which induces fatal acquired immunodeficiency syndrome (AIDS) in 100% (25 of 25) of persistently viremic experimentally infected specific pathogen-free (SPF) cats after predictable survival periods ranging from less than 3 months (acute immunodeficiency syndrome) to greater than one year (chronic immunodeficiency syndrome), depending on the age of the cat at time of virus exposure. The pathogenesis of FeLV-FAIDS-induced feline immunodeficiency disease is characterized by: a prodromal period of largely asymptomatic viremia; progressive weight loss, lymphoid hyperplasia associated with viral replication in lymphoid follicles, lymphoid depletion associated with extinction of viral replication in lymphoid follicles, intractable diarrhea associated with necrosis of intestinal crypt epithelium, lymphopenia, suppressed lymphocyte blastogenesis, impaired cutaneous allograft rejection, hypogammaglobulinemia, and opportunistic infections such as bacterial respiratory disease and necrotizing stomatitis. The clinical onset of immunodeficiency syndrome correlates with the replication of a specific FeLV-FAIDS viral variant, detected principally as unintegrated viral DNA, in bone marrow, lymphoid tissues, and intestine. Two of seven cats with chronic immunodeficiency disease that survived greater than 1 year after inoculation developed lymphoma affecting the marrow, intestine, spleen, and mesenteric nodes. Experimentally induced feline immunodeficiency syndrome, therefore, is a rapid and consistent in vivo model for prospective studies of the viral genetic determinants, pathogenesis, prevention, and therapy of retrovirus-induced immunodeficiency disease.
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PMID:Experimental transmission and pathogenesis of immunodeficiency syndrome in cats. 282 40

Normal mice infected with 10(5) infectious doses of lymphocytic choriomeningitis virus (LCMV, WE isolate) generated a reduced or no T cell-independent IgM and/or T cell-dependent IgG response to a subsequent vesicular stomatitis virus Indiana (VSV-IND) injection; this transient immune suppression lasted for weeks to months. Connatally infected LCMV-carrier mice or acutely infected T cell-deficient nude mice had normal anti-VSV IgM and IgG or IgM responses respectively. LCMV-infected nude mice transfused with helper cell-depleted LCMV-specific immune spleen cells were immunosuppressed. Normal mice infected with LCMV but treated with a rat anti-CD8 mAb (that had been shown previously to eliminate cytotoxic T cells in vivo) and then infected with VSV exhibited a normal anti-VSV IgM and IgG response. Since no IFN-alpha or -beta was detected on, or after, day 6 of LCMV infection, neither LCMV alone, nor IFN induced by it caused the observed immune suppression; the presented evidence suggests that LCMV-immune CD8+ T cells were responsible for it. It is conceivable that a similar pathogenesis where virus-specific cytotoxic T cells may destroy virus-infected cells essentially involved in an immune response (APC, T helper cells, etc.) may be involved in other virally triggered immune suppression or in AIDS.
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PMID:Virus-triggered immune suppression in mice caused by virus-specific cytotoxic T cells. 296 46

Human T-lymphotropic virus type III (LAV, HTLV-III) is aetiologically linked to acquired immune deficiency syndrome (AIDS) and persistent general lymphadenopathy (PGL). Specific radioimmunoassays (RIA), enzyme-linked assays, immunofluorescence assays (IFA) and immunoblotting techniques are being used widely to detect serum antibodies to HTLV-III in infected patients and in those at risk of infection. However, these assays do not functionally identify those antibodies that neutralize the infectivity of the virus. We have used three methods of titrating serum neutralizing factors: inhibition of syncytium induction, neutralization of envelope pseudotypes of vesicular stomatitis virus (VSV) and reduction of infectivity of HTLV-III for a cell line permissive to virus replication. We report here that sera from subjects in various disease categories possess only low-level neutralizing activity, even when antibodies to viral membrane antigens are present in high titre. Envelope pseudotypes prepared from four HTLV-III isolates made in three different countries are equally sensitive to neutralization by positive sera, including sera from patients yielding two of the virus isolates.
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PMID:Neutralization of human T-lymphotropic virus type III by sera of AIDS and AIDS-risk patients. 298 6

In addition to abnormalities in systemic immune function, patients with the acquired immunodeficiency syndrome (AIDS) and the pre-AIDS syndromes have significant abnormalities in the distribution of T-cell subsets in the intestinal tract. Such immune deficits predispose such patients to opportunistic infections and tumors, many of which involve the gastrointestinal tract. For example, Candida albicans often causes stomatitis and esophagitis. Intestinal infections with parasites (Cryptosporidium, Isospora belli, Microsporidia) or bacteria (Mycobacterium avium-intracellulare) are associated with severe diarrhea and malabsorption, whereas viruses like cytomegalovirus and herpes simplex virus cause mucosal ulcerations. Clinically debilitating chronic diarrhea develops in many AIDS patients for which no clear cause can be identified. Enteric pathogens like Salmonella and Campylobacter can be associated with bacteremias. Kaposi's sarcoma and lymphoma involving the intestinal tract are now well-recognized complications of AIDS. Although AIDS is not associated with a pathognomonic liver lesion, opportunistic infections and Kaposi's sarcoma or lymphoma may involve the liver.
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PMID:Gastrointestinal manifestations of the acquired immunodeficiency syndrome. 382 11

An immunologic profile may be useful to predict the development of Acquired Immune Deficiency Syndrome (AIDS) in both high risk patient groups including homosexuals, hemophiliacs, Haitians, and users of illicit intravenous narcotics as well as the general population. We evaluated 76 consecutive, apparently healthy, adults with congenital bleeding disorders for serum beta-2 microglobulin concentration by competitive enzyme immunoassay, T-lymphocyte subpopulations with monoclonal antibodies and serum interferon by inhibition of vesicular stomatitis virus plaque forming units. Findings on physical examination were remarkable with 24% of the group having longstanding splenomegaly and 24% lymphadenopathy. beta-2 microglobulin levels were 3232 +/- 220 micrograms/l (mean +/- SEM) with normal controls 2134 +/- 119 micrograms/l. The ratio of Leu3a (helper/inducer) positive to Leu2a (suppressor/cytotoxic) positive T-lymphocytes was 1.33 +/- 0.1 (mean +/- SEM, median = 1.18). Normal control ratios were all greater than 1.35 with a mean +/- s.d. = 1.96 +/- 0.28. Abnormal ratios of T-lymphocyte subpopulations appeared to persist over time. Increases in beta-2 microglobulin correlated with an inverted helper/suppressor T-lymphocyte ratio, the presence of lymphadenopathy, and elevations in aspartate aminotransferase. Interferon was detected in 18% of patient sera. More frequently transfused and more severely affected patients had a higher frequency of immunologic abnormalities although abnormalities also occurred in some rarely and never transfused less severely affected patients. These studies document a high incidence of immunologic abnormalities in patients with inherited coagulation defects.
AIDS Res
PMID:Immunologic profiles of adults with congenital bleeding disorders. 608 22


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