AJTMH HINARI
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am. J. Trop. Med. Hyg., 14(5), 1965, pp. 697-699
Copyright © 1965 by The American Society of Tropical Medicine and Hygiene

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lunn, J. S.
Right arrow Articles by Coatney, G. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lunn, J. S.
Right arrow Articles by Coatney, G. R.

Antibody Production in Plasmodium Vivax Infections Suppressed by Weekly Doses of Chloroquine

Joseph S. Lunn*, Richard L. Jacobs{dagger}, Peter G. Contacos{ddagger} AND G. Robert Coatney{dagger}

Five human volunteers were given weekly suppressive treatment with chloroquine (300 mg base) and then challenged with sporozoite induced Chesson strain vivax malaria. Therapy was continued for 4 to 6 weeks after exposure. Three non-medicated volunteers served as controls. Sera from each of the volunteers were subjected to tests for antibodies by the fluorescent antibody technique and for the determination of chloroquine levels.

All medicated volunteers maintained a chloroquine level of over 10 micrograms per liter during the period of therapy, with one exception. In this volunteer, on day 15 after exposure to malaria and 7 days after the previous dose of drug, the chloroquine level fell to 6 micrograms per liter.

Antibodies were first present in the controls and in 4 of the medicated volunteers 2 to 9 days after the onset of patent parasitemia. In the medicated volunteer whose chloroquine level fell below 10 µg/liter, antibodies developed while the patient was still receiving chloroquine.

It was suggested that the early appearance of antibodies in the one medicated volunteer was due to a transient subpatent parasitemia during a period of low serum-chloroquine level. It was concluded that circulating antibodies to erythrocytic parasites were not produced as a result of exoerythrocytic infection.


* Present address: Department of Medicine, University Hospital, Syracuse 10, New York.


{dagger} Laboratory of Parasite Chemotherapy, NIAID, National Institutes of Health, Bethesda, Maryland.


{ddagger} Medical Officer-in-Charge, Malaria Project, LPC, NIAID, NIH, U. S. Penitentiary, Atlanta, Georgia.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1965 by the American Society of Tropical Medicine and Hygiene.