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Journal of Clinical Microbiology, April 2001, p. 1416-1421, Vol. 39, No. 4
0095-1137/01/$04.00+0   DOI: 10.1128/JCM.39.4.1416-1421.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Biotyping of Penicillium marneffei Reveals Concentration-Dependent Growth Inhibition by Galactose

Samson S. Y. Wong,1 Timothy Y. C. Ho,2 Antonio H. Y. Ngan,1 Patrick C. Y. Woo,1 Tak-Lun Que,2 and Kwok-Yung Yuen1,*

Division of Infectious Disease, Department of Microbiology, The University of Hong Kong,1 and Department of Microbiology, Tuen Mun Hospital,2 Hong Kong

Received 5 September 2000/Returned for modification 12 November 2000/Accepted 11 January 2001

Thirty-two isolates of the dimorphic fungus Penicillium marneffei were studied for their biochemical properties. All isolates possessed the enzyme urease and were inhibited by 500 mg of cycloheximide per liter. No strain fermented glucose, and thus no strain fermented any of the other five sugars tested. All assimilated glucose, maltose, and cellobiose; only one of the isolates did not assimilate salicin. Totals of 65.6, 84.4, and 71.9% of the isolates assimilated trehalose, xylose, and nitrate, respectively. Twelve strains possessed the enzyme beta -galactosidase. Overall, 17 different biotypes were recognized, but no association was found between the human immunodeficiency virus status of the patients and the biotype. A novel finding of concentration-dependent growth inhibition of P. marneffei by galactose is described. Inhibition of growth occurred at a low concentration of galactose (0.015 to 0.25%) when galactose was the sole carbon source in the medium. Morphological changes of the fungal cells were observed in the presence of galactose.


* Corresponding author. Mailing address: Division of Infectious Disease, Department of Microbiology, Hong Kong University-Pasteur Research Centre, University Pathology Building, Queen Mary Hospital, 102 Pokfulam Rd., Hong Kong. Phone: (852) 2855 4892. Fax: (852) 2855 1241. E-mail: kyyuen{at}hkucc.hku.hk.


Journal of Clinical Microbiology, April 2001, p. 1416-1421, Vol. 39, No. 4
0095-1137/01/$04.00+0   DOI: 10.1128/JCM.39.4.1416-1421.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.



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