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It is uncertain whether HTLV-I infection and Strongyloidiasis are related other than by chance. A consecutive series of Jamaican patients and controls have been analysed retrospectively for anti-Strongyloides and HTLV-1 antibodies to determine whether either influences the outcome of anti-helminthic therapy. Twenty-seven Jamaicans (16 M, 11F) mean age 50.2 years (range 16-85), who were found to have Strongyloides stercoralis infection were studied at the University Hospital of the West Indies. At the same time, a parasite-negative group of 13 patients (6M, 7F) of mean age 37.6 years, (range 23-53), with minor or no gastrointestinal disease served as controls. Pretreatment blood samples were taken from the Strongyloides group and controls. Serum was subsequently tested for IgG antibodies to filariform Strongyloides stercoralis larval antigens by ELISA and to HTLV-1 by ELISA and Western Blot. Outcome of the treatment of Strongyloidiasis with thiabendazole (25 -mg/kg b.d. orally for 10 days was determined at 2 months. Strongyloides reciprocal antibody titre was considerably higher in patients than controls, mean 870 vs 167; median 1,024 vs 8 (p<0.001). The sensitivity of the antibody test was 93 percent, but the specificity was 69 percent at best. There was no correlation with the anti-Strongyloides antibody titre and outcome with anti-helminthic therapy. HTLV-1 antibodies were found only in the Strongyloides patients, 12 of 27 (44 percent); antibody titres were high and positive with both test used: only one patient was known beforehand to have a disease associated with HTLV-1 infection. Of those 12 with HTLV-1 antibodies, 3 (25 percent) were cured, 7 still had the infection at 2 months, a further 2 had died or defaulted from follow-up. Of the 15 patients without HTLV-1 antibodies, 9 (60 percent) were cured, 3 still had the infection and 3 had died or defaulted. By chi-square analysis, the difference is significant whether one includes all the deaths and defaulters on an intention-to-treat basis or just those who were available at 2 months post-therapy. However, since none of the deaths were related to Stongyloidiasis or HTLV-1 injection, it is probably justifiable to exclude the deaths from the computation. These results show that the association of Strongyloidiasis and HTLV-1 is more than chance clustering. Not only is the prevalence of HTLV-1 antibodies far higher in the patients with Strongyloidiasis than in the normal Jamaican population, but that concurrent asymptomatic HTLV-1 infection interferes with anti-helminthic treatment (AU)

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It was previously shown that malnourished Jamaican children often had evidence of selenium deficiency, viz. low erythrocyte glutathione peroxidase (RBC GSH Px) activity that correlated inversely with cardiothoracic ratio, and was particularly low in children who died. In this study, RBC GSH Px activity, plasma GSH Px activity and plasma selenium concentration were measured in 41 malnourished children on admission to hospital, and after recovery in weight-for-height. Plasma GSH Px activity and selenium concentrations were also measured longitudinally throughout recovery in a group of 24 initially selenium-deficient children, 17 of whom were given oral selenium supplements for the first 3 weeks. RBC GSH Px activity was low in all malnourished children, whether oedematous or not (Table). It did not change with recovery. Plasma GSH Px activity and plasma selenium concentration were low only in oedematous malnourished children. PEM GROUPS: control, marasmus, oedematous; ERYTHROCYTE GSH Px (U/gHb)- *36ñ2, 24ñ4, 21ñ3 respectively; PLASMA GSH Px act. (U/L) - 140ñ9, 142ñ15, 98ñ8 respectively, PLASMA SE CONCN. (æg/e) - 86ñ4, 76ñ12, 53ñ5. *meanñSEM. Selenium was associated with a rapid rise in both plasma GSH Px activity and plasma selenium concentration. The increase in plasma selenium was more dramatic (44 up to 144 æg/e in 6 days): the variability in plasma GSH Px activity was much greater, and they remained within the control range. The changes were sustained after supplementation ceased. We conclude that (1) selenium deficiency in malnourished Jamaican children is not reversed during 'recovery' on the conventional 'high energy' diet, (2) plasma selenium concentration responds rapidly to changes in selenium intake, and is a useful measure of selenium status, and (3) oral selenium supplements improve selenium status in children recovering from malnutrition (AU)

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Two patients with chronic Strongyloidiasis, refractory to conventional therapy, were studied by whole gut irrigation and high-dose antihelminthic therapy. Saline (0.9 percent) was given via naso-gastric tube at 50 ml per minute. After solid material was cleared, the gut effluent was collected in 10-minute samples. After one hour baseline collection, mebendazole (1,800 mg in patient 1) or levamisole (1,100 mg in patient 2) was given. Irrigation and collection continued for a further 140 and 170 minutes respectively. Parasitic forms were collected and counted in each sample. In the mebendazole treated patient the spontaneous egg- and larval-shedding rate was 1,501/minute. This was not affected by mebendazole treatment. Adults first appeared in the effluent at 1 hour after treatment and the numbers were increasing at the termination of the infusion. Nineteen adults were recovered. Follow-up showed no diminution in the intensity of infection, demonstrating that only a small proportion of the available adults had been recovered or expelled. In the levamisole treated patient, the pre-treatment effluent contained 49,041 larvae/minute and no adult forms. In contrast to mebendazole, after treatment with levamisole, there was a massive efflux of adults which had not returned to baseline after 3 hours; 88,729 adults were recovered. The post-treatment infection level was reduced dramatically and a further 15,000 adults were recovered within 24 hours. There was no increase in larval output with levamisole. It is concluded that neither mebendazole nor levamisole has a direct on Strongyloides larvae. However, they are both active against the adult forms, with the potency of levamisole appearing to be greater than that of mebendazole. Treatment with these drugs may have to continue for longer than the full maturation time of endogenous larvae. This may be in excess of 4 weeks (AU)

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