Nonenterotoxigenic strains no. 1196-78 and no. 1074-78 of Vibrio cholerae serogroup O1 (biotype El Tor, serotype Ogawa) were isolated from sewage water in Brazil and fed to 20 volunteers. Neither strain caused diarrhea. None of the seven volunteers who ingested Ogawa strain no. 1074-78 (10(6) organisms) excreted the organism whereas eight of the 13 volunteers who ingested Ogawa strain no. 1196-78 (10(6) or 10(8) organisms) did excrete the organism in their stools. None of 114 stool-culture isolates yielded cholera enterotoxin, and none of the 20 volunteers had significant increases in serum titers of antitoxin as measured by enzyme-linked immunosorbent assay although six of the volunteers had slightly elevated vibriocidal antibody levels. Six volunteers used as controls and four volunteers who had stool cultures positive for strain no. 1196-78 of V. cholerae were challenged with pathogenic El Tor Ogawa strain no. E7946 (10(6) organisms) to determine if previous ingestion of the Brazilian strain would induce protective immunity. All 10 of the volunteers developed diarrhea, and the severity of the illness was similar in both groups.
To assess the risk of nosocomial transmission of human T-cell lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV), we prospectively evaluated a cohort of 531 health care workers. One hundred fifty of these employees reported percutaneous or mucous membrane exposures to blood or body fluids from a patient with the acquired immunodeficiency syndrome (AIDS) during the treatment of 238 such patients since 1981. None of these 150 employees had serologic evidence of HTLV-III/LAV infection on follow-up from 6 to 46 months after exposure. Of the 150, 46 were studied immunologically and 29 had lymphocytes cultured for HTLV-III/LAV. Results of all studies were normal. Of the 531 employees, 3 (0.56%) had serologic evidence of HTLV-III/LAV infection. All were seropositive at the time of study entry; none reported adverse nosocomial exposures. All acknowledged membership in one or more established risk groups for AIDS. This study provides strong evidence that the risk of nosocomial transmission of HTLV-III/LAV is extremely low.
The possibility that an agent in addition to the human immunodeficiency virus (HIV) may contribute to the etiology of non-Hodgkin's lymphoma in persons with acquired immunodeficiency syndrome (AIDS) was studied using participants from the Multicenter AIDS Cohort Study (MACS) of homosexual and bisexual men enrolled in 1984-1985 and also in 1987-1991. A nested case-control analysis was conducted. The primary source of information on potential exposures and characteristics of the participants was the baseline study entry interview that was conducted prior to the development of AIDS. A total of 84 cases of non-Hodgkin's lymphoma were identified and compared with 527 participants who developed AIDS but had no evidence of cancer. The groups were similar for most sociodemographic characteristics as well as sexual activity and past history of antecedent illnesses. Although the non-Hodgkin's lymphoma cases reported less frequent use of recreational drugs and cigarettes compared with other persons with AIDS, these differences were not significant. Non-Hodgkin's lymphoma cases reported more frequent intake of aspirin during the week before the interview. However, there were no differences between the comparison groups for long-term aspirin intake or intake of other analgesics. The absence of any specific and strong association between non-Hodgkin's lymphoma and the various behavior-related activities and exposures considered in this analysis suggests that these factors are not related to a second agent in the etiology of HIV-induced non-Hodgkin's lymphoma. The possibility that a very common agent in this study population or that differences in the nature of the immune dysfunction resulting from HIV infection could act as a cofactor for HIV-induced non-Hodgkin's lymphoma cannot be excluded.
For patients who began receiving zidovudine during intermediate-stage disease, changing to either combination therapy or sequential monotherapy was associated with a statistically significant survival benefit compared with continuation of zidovudine monotherapy. The absolute increase in survival was modest, however, and long-term survival remained poor. Simultaneous time-dependent adjustment for changes in therapy and in important prognostic variables is necessary to derive relatively unbiased estimates of treatment effects in observational studies of HIV infection.
We determined intrathecal synthesis (ITS) of anti-HIV-1 immunoglobulin in 62 CSF samples from 51 HIV-1 seropositive homosexual men using an ELISA technique with paired serum and CSF samples diluted to a concentration of IgG of 10 micrograms/ml. All subjects were neurologically normal and none was taking zidovudine. We estimated duration of HIV-1 infection from semiannual serologic testing during the 3-year period before CSF analysis and detected ITS of anti-HIV-1 immunoglobulin in 2 of 12 (17%) of those with less than 18 months of HIV-1 seropositivity, in 3 of 21 (14%) with 19 to 36 months, and in 13 of 29 (45%) with greater than 36 months of HIV-1 seropositivity (p = 0.037). There was a trend toward an inverse relationship between level of ITS and the peripheral blood T-helper lymphocyte count. This study demonstrates that increasing ITS of anti-HIV-1 IgG is related to duration of HIV-1 infection and suggests an inverse correlation with systemic immune status. The detection of ITS of anti-HIV-1 immunoglobulin is not necessarily a marker of clinically overt neurologic involvement.
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