{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T10:17:23Z","timestamp":1784715443783,"version":"3.55.0"},"reference-count":10,"publisher":"American Society for Microbiology","issue":"5","license":[{"start":{"date-parts":[[2005,5,1]],"date-time":"2005-05-01T00:00:00Z","timestamp":1114905600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Clin Vaccine Immunol"],"published-print":{"date-parts":[[2005,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>We report strongyloides hyperinfection in two patients with generalized hypogammaglobulinemia from multiple myeloma and nephrotic syndrome, despite a significant strongyloides-specific immunoglobulin G (IgG) response. In contrast to reports on animals, where human IgG was shown to be a protective antibody, our observation suggests that in humans, immunity to the infective-stage larvae is not protective against the autoinfective larvae, which are the causative agents of strongyloides hyperinfection.<\/jats:p>","DOI":"10.1128\/cdli.12.5.680-682.2005","type":"journal-article","created":{"date-parts":[[2005,5,5]],"date-time":"2005-05-05T17:23:00Z","timestamp":1115313780000},"page":"680-682","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":16,"title":["Strongyloides Hyperinfection and Hypogammaglobulinemia"],"prefix":"10.1128","volume":"12","author":[{"given":"Raymond C. 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