{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,11]],"date-time":"2026-11-11T03:10:49Z","timestamp":1794366649415,"version":"4.9.0"},"reference-count":13,"publisher":"American Society for Microbiology","issue":"6","license":[{"start":{"date-parts":[[2002,6,1]],"date-time":"2002-06-01T00:00:00Z","timestamp":1022889600000},"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":["J Clin Microbiol"],"published-print":{"date-parts":[[2002,6]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Botulism results from consumption of preformed toxin or in vivo toxin elaboration in wounds or intestine. Of U.S. food-borne botulism cases since 1950, the majority were due to toxin A, but a significant number of suspect cases were never confirmed by culture or toxin detection. We report here a possible case of food-borne botulism attributed to toxin F production by a\n            <jats:italic>Clostridium baratii<\/jats:italic>\n            organism isolated from food consumed by the patient. The isolation of a toxin-producing\n            <jats:italic>Clostridium<\/jats:italic>\n            species other than\n            <jats:italic>Clostridium botulinum<\/jats:italic>\n            from food and stool requires deviation from the usual laboratory protocols, which may account for the lack of complete laboratory confirmation of clinically diagnosed cases.\n          <\/jats:p>","DOI":"10.1128\/jcm.40.6.2260-2262.2002","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T10:09:29Z","timestamp":1027764569000},"page":"2260-2262","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":72,"title":["Botulism Due to\n            <i>Clostridium baratii<\/i>\n            Type F Toxin"],"prefix":"10.1128","volume":"40","author":[{"given":"Sydney M.","family":"Harvey","sequence":"first","affiliation":[{"name":"Public Health Laboratory"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joan","family":"Sturgeon","sequence":"additional","affiliation":[{"name":"Public Health Laboratory"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David E.","family":"Dassey","sequence":"additional","affiliation":[{"name":"Acute Communicable Disease Control Unit, County of Los Angeles Department of Health Services, Los Angeles, California"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_1_2_2","first-page":"654","year":"1999","unstructured":"Allen, S. D., C. L. Emery, and J. A. Siders. 1999. Clostridium, p. 654-671. In P. R. Murray, E. J. Barron, M. Q. Pfaller, F. C. Tenover, and R. H. Yolken (ed.), Manual of clinical microbiology. American Society for Microbiology, Washington, D.C.","journal-title":"Manual of clinical microbiology"},{"key":"e_1_3_1_3_2","doi-asserted-by":"publisher","DOI":"10.1093\/infdis\/154.2.207"},{"key":"e_1_3_1_4_2","unstructured":"Centers for Disease Control and Prevention. 1998. Botulism in the United States 1899-1996: handbook for epidemiologists clinicians and laboratory workers. Centers for Disease Control and Prevention Atlanta Ga."},{"key":"e_1_3_1_5_2","unstructured":"Doyle M. P. 1989. Foodborne bacterial pathogens p. 147. Marcel Dekker Inc. New York N.Y."},{"key":"e_1_3_1_6_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1574-6968.1992.tb05421.x"},{"key":"e_1_3_1_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/jcm.21.4.654-655.1985"},{"key":"e_1_3_1_8_2","first-page":"3","volume":"54","year":"1993","unstructured":"Hatheway, C. L. 1993. Clostridium botulinum and other clostridia that produce botulinum neurotoxin. Food Sci. Technol. (New York)54:3-20.","journal-title":"Food Sci. Technol. 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