Measles and immune globulin prophylaxis for travelers and hepatitis A.
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Biomedical subjects
Publications and source records attributed to M S Wolfe.
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Exotic infections are a significant threat to the child traveling to or going to live in the developing world. Vaccines are available that can prevent some of these infections. It is essential that basic routine childhood vaccination be up to date and that necessary modifications be made from the usual schedule in the United States. The current requirements and local disease conditions (both endemic and epidemic) for each country to be visited must be known so that appropriate vaccines are received. Resources for this information are listed. Details for each vaccine are given, including indications, dose, booster, side effects, contraindications, and other specific information.
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A cohort of 169 births to women who were exposed throughout pregnancy to chloroquine 300 mg base once a week for chemosuppression of malaria was studied. The birth defects in this cohort were compared with those in a control group of 454 births to women who were not exposed to chloroquine, most of whom lived in non-malarious areas. The proportion of birth defects in the exposed group was not significantly different from that in the control group. This observation must be considered within the limitations of the study, which could detect only a strong teratogenic effect. It could not exclude risks lower than a 5.7-fold increase in the incidence of birth defects when chloroquine was used. Women using chloroquine during pregnancy for chemosuppression of malaria can be reassured that it is not a strong teratogen, but if it is to be used the risk of developing malaria should be balanced against the lack of data to determine whether it carries a low teratogenic risk.
An American Peace Corps volunteer contracted chloroquine-resistant Plasmodium falciparum malaria while serving in Malawi and taking regular chloroquine prophylaxis. Resistance was confirmed by in vitro testing of his parasites for chloroquine and pyrimethamine. The possibility of Fansidar-resistant falciparum malaria was also suggested in this case. American expatriates residing in or traveling to Malawi are advised to either take both chloroquine and Fansidar, or alternatively amodiaquine or doxycycline alone. Any breakthrough of slide-proven falciparum malaria in these individuals should be seriously suspected to be chloroquine- and Fansidar-resistant malaria, and should be treated with quinine and tetracycline.
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Spondweni virus is a mosquito-borne flavivirus previously reported to cause human disease in Southern and West Africa. A serologically confirmed case of Spondweni virus infection in a U.S. citizen residing in Upper Volta is reported. Symptoms included fever, chills, headache, myalgia, nausea, and rash. A greyish mucoid lining was present on the posterior pharynx. The differential diagnosis included rickettsial infection, leptospirosis, typhoid fever, and numerous viral illnesses including Lassa fever. Evidence of Spondweni virus infection was also found in two other U.S. citizens residing in Gabon and Cameroon. Spondweni virus might be a cause of acute febrile illness throughout West Africa, and its presence should be considered in the differential diagnosis of febrile illness and in antibody surveys in that region.
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Two cases of serum sickness from furazolidone (Furoxona), prescribed for giardiasis in Latin America, are described. No previous case of serum sickness related to this drug has been reported in the United States. Tartrazine (yellow dye number 5), a component of furazolidone tablets (Furoxona) manufactured in Latin America countries but no longer included in the drug (Furoxone) in the United States is suggested as a possible cause of serum sickness.
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Cytosol prepared from epididymides of sexually immature (21-23-day-old) rats contains a macromolecular binding component for estradiol-17 beta. This binding moiety sediments as an 8-S species on 5-20% sucrose gradients containing 0.01 M KCl. Under conditions of high ionic strength (0.4 M KCl) the 8-S peak of estradiol binding is shifted to the 4-S region, suggesting dissociation of receptor aggregates. Time-course studies indicated that binding equilibrium was essentially achieved after 2 hours incubation at 0 degrees C. Although unlabeled estrone and estriol are capable of inhibiting [3H]estradiol binding to epididymal cytosol, they are less effective than unlabeled estradiol. Unlabeled 5 alpha-dihydrotestosterone (5 alpha-DHT) at a 100-fold molar excess did not cause a statistically significant inhibition of [3H]estradiol binding. Unlabeled estrogens, but not unlabeled 5 alpha-DHT or cortisol (at the concentrations used), were capable of displacint [3H]estradiol from its binding sites. The dissociation of [3H]estradiol from the binding component is very slow, with half-time of dissociation being greater than 16 hours. The epididymal estrogen binder is saturable at low concentrations of ligand. The dissociation constant was of the order of 10(-11)M and the concentration of binding sites was approximately 10(-14) mol/mg protein. This estrogen binder has the characteristics which are usually attributed to steroid receptors and is clearly different from the testicular androgen-binding protein and the epididymal androgen receptor.