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Volume 5, Number 1—February 1999
Dispatch

Mycoplasma penetrans Bacteremia and Primary Antiphospholipid Syndrome1

Antonio Yáñez*Comments to Author , Lilia Cedillo†, Olivier Neyrolles‡, Encarnación Alonso*, Marie-Christine Prévost‡, Jorge Rojas*, Harold L. Watson§, Alain Blanchard‡, and Gail H. Cassell§
Author affiliations: *Centro de Investigación Biomédica de Oriente-IMSS, Puebla City, Mexico;; †Benemérita Universidad Autónoma de Puebla, Puebla City, Mexico;; ‡Institut Pasteur, Paris, France;; §University of Alabama at Birmingham, Birmingham, Alabama, USA

Main Article

Figure 1

Polymerase chain reaction (PCR) detection of Mycoplasma penetrans in clinical samples. A. M. penetrans PCR genomic amplification with the primers MYCPENET-P and MYCPENET-N (7) and analyzed by electrophoresis in 2% agarose gel. Lysates from the following original samples: throat swab (lane 1); tracheal aspirate (lane 2); blood (lane 3); first blood subculture (HF-1 isolate) (lane 4); M. penetrans GTU-54-6A1 (lane 5), showing the amplification product of 407-bp; and negative control (lane 6). B. S

Figure 1. Polymerase chain reaction (PCR) detection of Mycoplasma penetrans in clinical samples. A. M. penetrans PCR genomic amplification with the primers MYCPENET-P and MYCPENET-N (7) and analyzed by electrophoresis in 2% agarose gel. Lysates from the following original samples: throat swab (lane 1); tracheal aspirate (lane 2); blood (lane 3); first blood subculture (HF-1 isolate) (lane 4); M. penetrans GTU-54-6A1 (lane 5), showing the amplification product of 407-bp; and negative control (lane 6). B. Southern blotting of the same material. Hybridization with the internal oligonucleotide (MYCPENET-S) probe confirmed the specific amplification of M. penetrans genetic sequences.

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1Presented in part at the 11th International Congress of the International Organization for Mycoplasmology. July 14–19, 1996. Orlando, FL, USA.

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