To evaluate modern treatment and identify important factors influencing the outcome of tuberculous meningitis, clinical and laboratory findings in 52 patients aged from 9 months to 68 years have been reviewed. Patients were classified by clinical criterions at admission and at the start of treatment. Delay in commencing treatment was associated with deterioration and consequently poorer prognosis, but some severely ill patients made a good recovery. Forty-four survivors (85%) recovered, and only two patients (4%) had severe residual disability; eight (15%) of the patients died. Treatment should commence as soon as possible on clinical grounds without necessarily waiting for demonstration of Mycobacterium tuberculosis, as the organism can often be demonstrated in CSF withdrawn after the start of drug therapy.

An enzyme-linked immunosorbent assay (ELISA) measuring IgA antibodies in the vaginal mucus was used to diagnose bovine venereal campylobacteriosis in 241 herds with infertility and abortions. The presence of the disease was confirmed on 84 farms (34.8%) and it was suspected on a further 27 farms (11.2%). The specificity of the ELISA was found to be 98.5% but in the absence of a reliable comparative test sensitivity can not be estimated. Vaccination against campylobacteriosis will not interfere with the IgA ELISA because only IgG is present in the vaginal mucus of vaccinates. Because of the possibility of false reactions caused by antibody fluctuations in individual cattle, the ELISA is best used as a herd test. It appears that at present the vaginal mucus IgA ELISA is the test of choice for the diagnosis of bovine venereal campylobacteriosis.

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Human immunodeficiency virus (HIV)-infected CD8 lymphocytes have been reported in vivo؉ CD4 ؊ lymphocytes (undetectable in seven of nine individuals; P < 0.01) and approached that of CD4 lymphocytes from the same individuals (median, 3,660 HIV LTR copies/10 6 cells). CD8 bright CD4 dim lymphocytes represented 0.8 to 3.3% of total CD8 lymphocytes and were most prevalent in the memory subset. Thus, HIV-infected CD8 lymphocytes commonly circulate in HIV-infected individuals and are generated through infection of activated CD8 lymphocytes rather than through export of intrathymically infected precursors. The high level of infection of CD8 bright CD4 dim lymphocytes could have a direct role in the decline in CD8 lymphocyte function that accompanies HIV disease progression.