BackgroundOral candidiasis is an infection caused by a yeast-like fungus called Candida. Various methods can be used to isolate Candida from the oral cavity. However, it is difficult to correctly and satisfactorily diagnose oral candidiasis because currently no microbiological or laboratory standards based on samples from the oral cavity are available. The aim of this study is to establish a reliable laboratory test for diagnosing oral candidiasis.MethodsOral swab, rinse and concentrated rinse samples were obtained from 200 consecutive outpatients (103 male patients and 97 female patients; mean age, 47.2 years; age range, 9–89 years). Candida colonies from cultured samples were enumerated to compare the sensitivities and specificities of the above sampling methods, and the associations between Candida detection or concentration and the clinical oral signs were examined.ResultsThe mean colony numbers were 263 ± 590 CFU/swab for the swab method, 2894 ± 6705 CFU/100 μL for the rinse method, and 9245 ± 19,030 CFU/100 μL for the concentrated rinse method. The median numbers were 23 CFU/swab for the swab method, 56 CFU/100 μL for the rinse method, and 485 CFU/100 μL for the concentrated rinse method. Candida was detected in the oral cavity of 33.5 % and 52.0 % of the outpatients by the swab method and concentrated rinse, respectively. Candida concentrations determined by the concentrated rinse were closely related to the severity of the clinical oral signs. The positive predictive values of residual root, redness of the oral mucosa, denture, glossalgia, dry mouth, and taste disorder were useful predictors of oral candidiasis.ConclusionsConcentrated rinse sampling is suitable for evaluating oral candidiasis, and Candida concentrations examined using this method strongly associated with the oral signs associated with Candida infection.

Haemophilus influenzae is a common pathogen of respiratory infections. We examined whether beta-lactamase-negative ampicillin-resistant (BLNAR) strains that are known to have ampicillin resistance due to a substitution of amino acid of penicillin binding protein (PBP)-3, differ from beta-lactamase-negative ampicillin-susceptible strains with regard to invasion of bronchial epithelium. After 3h incubation of each of 34 beta-lactamase-negative ampicillin-susceptible and 57 BLNAR strains in the presence of BEAS-2B cells, a human bronchial epithelium cell line, extracellular bacteria were killed using gentamicin and intracellular bacteria numbered. All nine strains in which the efficiency of invasion was 1% or higher were BLNAR strains. The rate of invasion was significantly greater in strains with PBP-3 amino acid substitution (Met377 to Ile, Ser385 to Thr, Leu389 to Phe, and Asn526 to Lys) (n=34) than in those with no amino acid substitution. Electron microscopy showed that high invasive BLNAR strains were observed in cytoplasm of BEAS-2B cell layer. The injured cells were 9.44+/-1.76% among attaching cells examined by trypan blue staining after 6h. These data may suggest that the amino acid substitution of the PBP in BLNAR strains may at least partly play roles in macropinocytosis, leading to the invasion and injury to epithelial cells.

An Ambler class A ␤-lactamase gene, bla CIA-1 , was cloned from the reference strain Chryseobacterium indologenes ATCC 29897 and expressed in Escherichia coli BL21. The bla CIA-1 gene encodes a novel extended-spectrum ␤-lactamase (ESBL) that shared 68% and 60% identities with the CGA-1 and CME-1 ␤-lactamases, respectively. bla CIA-1 -like genes were detected from clinical isolates. In addition to the metallo-␤-lactamase IND of Ambler class B, C. indologenes has a class A ESBL gene, bla CIA-1 , located on the chromosome.

The presence of anti-ETA antibodies below a particular cutoff level might be associated with SSSS onset in preterm infants.

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