Blastocystis is an enteric protozoan parasite commonly found in humans and animals. Phylogenetic and genotypic analyses have shown that Blastocystis exhibits extreme genetic diversity, and humans are host to a number of zoonotic isolates. In the present study, the prevalence of Blastocystis in 276 stool samples from a hospital in Singapore was examined, and for the first time, riboprinting using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to determine the genetic diversity of the Blastocystis isolated from the Singapore population. The prevalence rate was determined to be 3.3% (9/276), and Blastocystis displaying two main ribotypes were isolated. As a comparison, we performed PCR-RFLP using two different published methodologies, and both methods allowed the isolates to be divided into two distinct groups based on their riboprint patterns. According to a recently proposed classification scheme, 78% (7/9) of the isolates were of subtype 3, while 22% (2/9) were subtype 1. The predominance of subtype 3 in an urbanized city state such as Singapore is in agreement with the idea that subtype 3 is a genotype of human origin.
e c t i o n , Volume 5 N u m b e r 5 , M a y 1999 originated (data not shown), one would perhaps expect to see mutations being lost or gained within the genes potentially affecting quinolone susceptibility. The stability of mutations in genes known to be associated with fluoroquinolone resistance, and the stable MIC values in clonally related MRSA isolates over time, have important implications for quinolone resistance in S. aureus. From this study of clinical MRSA isolates, it seems likely that once acquired, mutations and the decreased susceptibility to quinolones that they confer are highly stable, suggesting that the high prevalence of fluoroquinolone resistance that we are experiencing today in some parts of the world will remain.
References1. Goldstein Nv, Acar JE Epidemiology of quinolone resistance: Europe and North and South America. Drugs 1995; 49 (suppl 2): 36-42. 2. Kaatz GW, Seo SM. Inducible norA-mediated multidrug resistance in Staphylococcus aureus. Antimicrob Agents Chemother 1995; 39: 2650-5. 3. Yoshida H, Bogaki M, Nakamura S, Ubukata K, Konno M. Nucleotide sequence and characterization of the Staphylococcus aureus norA gene which confers resistance to quinolones. J Bacteriol 1990; 172: 6942-9. 4. Brockbank SMV, Barth PT. Cloning, sequencing, and expression of the DNA gyrase genes from Staphylococcus aureus. J Bacteriol 5. Goswitz JJ, Wdlard KE, Fashing CE, Peterson LR. Detection of gyrA gene mutations associated with ciprofloxacin resistance in methicillin resistant Staphylococcus aureus: Analysis by polymerase chain reaction and automated DNA sequencing. Antimicrob Agents ChemotherIn the early 1990s, an increasing number of serogroup C meningococcal strains was observed [l], and a rise in the incidence of the disease was also found, especially in some regions in the northwest of the country,
Two Cryptococcus neoformans strains isolated from an AIDS patient were investigated, a pretreatment isolate (CN1) and a second isolate (CN3) following failure of fluconazole and amphotericin B treatment. No difference in fluconazole sensitivity, but relative resistance to amphotericin B was observed for CN3. The sterol composition of CN3 indicated a defect in sterol delta 8-->7 isomerase in this strain and depletion of ergosterol, the major sterol of the CN1.
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