Interferential therapy machines as possible vehicles for cross-infection.

Interferential therapy machines are used to apply alternating electric currents to patients for the treatment of various musculo-skeletal complaints. The potential for such machines to transfer skin microflora from one patient to another during treatment was investigated. The efficacy of the current disinfection procedure of the machines was also evaluated. In both the laboratory and clinical situation, interferential treatment, (which involves the direct application of electrodes to the skin surface) resulted in the transfer of micro-organisms from the skin of one subject to another. To decrease the likelihood of transmission of micro-organisms via interferential therapy machines, it is recommended that both the suction cups and sponges are disinfected with 70% isopropyl alcohol after the treatment of each patient. The use of disposable electrodes could also be considered.

Quinolinic acid in the cerebrospinal fluid of children with symptomatic human immunodeficiency virus type 1 disease: relationships to clinical status and therapeutic response.

Quinolinic acid (QUIN) is a neurotoxin implicated in the neurologic deficits associated with human immunodeficiency virus type 1 (HIV-1) infection. Forty children with symptomatic HIV-1 disease had elevated (P < .001) cerebrospinal fluid (CSF) QUIN levels (55.8 +/- 8.9 nM) compared with controls (14.9 +/- 3.0 nM). Age-adjusted CSF QUIN concentrations in HIV-1-infected children were predicted by the general index of mental abilities (GIMA, from an age-appropriate intelligence test; r = -0.45, P < .01). Zidovudine therapy reduced CSF QUIN from 64.1 +/- 16.3 to 19.7 +/- 5.2 nM (P < .01; N = 16) and increased GIMA from 76.8 +/- 5.2 to 87.2 +/- 6.3 (P < .001). Encephalopathic HIV-1-infected patients had higher CSF QUIN levels than patients without encephalopathy (79.6 +/- 16.1 vs. 32.7 +/- 6.7 nM, P < .01). CSF QUIN concentrations were also higher (P < .001) in patients who died < or = 3 years after their baseline assessment, compared with those who were still alive. These results warrant further investigation of CSF QUIN in HIV-infected children as a mediator of neurologic dysfunction and a supplemental marker of neurologic disease, particularly when combined with measures of neurocognitive functioning.