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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

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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.

Main Article

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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