Idiopathic CD4+ T-lymphocytopenia--four patients with opportunistic infections and no evidence of HIV infection.

BACKGROUND AND METHODS: We describe four patients without major risk factors for human immunodeficiency virus (HIV) infection, each of whom presented with severe opportunistic infections and was found to have idiopathic CD4+ T-lymphocytopenia. We performed assays to detect the presence of retroviruses and undertook immunophenotyping of subgroups of peripheral-blood lymphocytes. RESULTS: The opportunistic infections at presentation included Pneumocystis carinii pneumonia, cryptococcal meningitis (two patients, one with concurrent pulmonary tuberculosis), and histoplasma-induced brain abscess. During 10 to 68 months of observation, none of the four patients had evidence of infection with HIV type 1 or 2 or human T-cell lymphotropic virus type I or II on the basis of epidemiologic, serologic, or polymerase-chain-reaction studies or culture, nor was there any detectable reverse transcriptase activity. Although all the patients had severe, persistent CD4+ T-lymphocytopenia (range, 12 to 293 cells per cubic millimeter), the CD4+ cell count progressively declined in only one and was accompanied by multiple opportunistic infections. All four patients had significantly reduced numbers of circulating CD8+ T cells, natural killer cells, or B cells (or all three). CONCLUSIONS: These four patients had idiopathic CD4+ T-lymphocytopenia with opportunistic infections but no evidence of HIV infection. Instead of the progressive, selective depletion of CD4+ T cells characteristic of HIV infection, some patients with idiopathic immunodeficiency have stable CD4+ cell counts accompanied by reductions in the levels of several other lymphocyte subgroups.

Comparison of cefoperazone with penicillin, ampicillin, gentamicin, and chloramphenicol in the therapy of experimental meningitis.

Cefoperazone was compared with penicillin against Streptococcus pneumoniae, gentamicin against Escherichia coli, and ampicillin and chloramphenicol against Haemophilus influenzae in the therapy of experimental meningitis in rabbits. Meningitis was produced by intracisternal inoculation into cerebrospinal fluid, and all antibiotics were administered intravenously over 8 h in dosages that would achieve serum levels comparable to those found in humans. The mean percent penetration into purulent cerebrospinal fluid, expressed as (cerebrospinal fluid concentration/serum concentration) x 100%, was 2.6% for penicillin, 22.0% for gentamicin, 12.1% for ampicillin, 23.8% for chloramphenicol, and 6.4% for cefoperazone. The mean cerebrospinal fluid antibiotic concentrations exceeded the minimum bactericidal concentration for the test strain in each experimental model, except for ampicillin in experimental meningitis due to the beta-lactamase-producing H. influenzae. Cefoperazone produced a significantly faster bactericidal effect after 4 h of treatment when compared with penicillin (P = 0.037) and ampicillin (P = 0.01) in meningitis caused by S. pneumoniae and H. influenzae (ampicillin susceptible), respectively. In meningitis caused by E. coli, cefoperazone was significantly (P = 0.006) more rapidly bactericidal after 8 h of treatment when compared to gentamicin. In addition, cefoperazone was significantly more rapidly bactericidal than either ampicillin or chloramphenicol in experimental meningitis due to beta-lactamase-producing H. influenzae. Cefoperazone deserves further evaluation in the therapy of bacterial meningitis in humans.