A cluster of Candida krusei infections in a haematological unit.

BACKGROUND: Candida krusei infections are associated with high mortality. In order to explore ways to prevent these infections, we investigated potential routes for nosocomial spread and possible clonality of C. krusei in a haematological unit which had experienced an unusually high incidence of cases. METHODS: We searched for C. krusei contamination of the hospital environment and determined the level of colonization in patients and health care workers. We also analyzed the possible association between exposure to prophylactic antifungals or chemotherapeutic agents and occurrence of C. krusei. The C. krusei isolates found were genotyped by pulsed-field electrophoresis method in order to determine possible relatedness of the cases. RESULTS: Twelve patients with invasive C. krusei infection and ten patients with potentially significant infection or mucosal colonization were documented within nine months. We were unable to identify any exogenic source of infection or colonization. Genetic analysis of the isolates showed little evidence of clonal transmission of C. krusei strains between the patients. Instead, each patient was colonized or infected by several different closely related genotypes. No association between medications and occurrence of C. krusei was found. CONCLUSION: Little evidence of nosocomial spread of a single C. krusei clone was found. The outbreak may have been controlled by cessation of prophylactic antifungals and by intensifying infection control measures, e.g. hand hygiene and cohorting of the patients, although no clear association with these factors was demonstrated.

Proteolytic Mediators in Gestational Diabetes Mellitus and Gingivitis.

BACKGROUND: This study evaluates levels of matrix metalloproteinase (MMP)-8, MMP-9, and tissue inhibitor of MP-1 (TIMP-1) in biofluids of women with gestational diabetes mellitus (GDM) and systemically healthy counterparts with different statuses of periodontal health. METHODS: Seventy-one women with GDM and gingivitis (Gg), 30 women with GDM and healthy periodontium (Gh), 28 systemically and periodontally healthy women (Hh), and 37 systemically healthy women with gingivitis (Hg) were evaluated. MMP-8, MMP-9, and TIMP-1 levels were determined in gingival crevicular fluid (GCF), saliva, and serum by immunofluorometric and enzyme-linked immunosorbent assays. Full-mouth clinical periodontal parameters were recorded. RESULTS: GCF and serum MMP-8 concentrations, serum MMP-9 concentrations, and serum MMP-8/MMP-1 and MMP-9/MMP-1 molar ratios were significantly higher in Gg compared with Hg group (P <0.05). Serum MMP-8 levels and salivary TIMP-1 levels were higher in Gh compared with Hg group (P <0.05) whereas salivary MMP-8/TIMP-1 molar ratio was lower in Gh compared with Hg group (P <0.05). Elevated concentrations of GCF MMP-8 and MMP-9 were found in Gg compared with Gh group (P <0.05). Significant correlations were found between local levels of biomarkers and clinical periodontal parameters in only GDM group. CONCLUSION: GDM may modulate both local and circulating levels of MMP-8 especially when associated with gingivitis.

Gingival Inflammation and Salivary or Serum Granulocyte-Secreted Enzymes in Patients With Polycystic Ovary Syndrome.

BACKGROUND: The objective of this cross-sectional study is to investigate levels of salivary and serum matrix metalloproteinase (MMP)-9, myeloperoxidase (MPO), neutrophil elastase (NE), and MMP-9/tissue inhibitor of MMP-1 (TIMP)-1 ratio in patients with polycystic ovary syndrome (PCOS) and systemically healthy controls in the presence or absence of gingivitis. METHODS: Serum and salivary levels of these biomarkers were evaluated in the following: 1) periodontally healthy women with PCOS (n = 45); 2) women with PCOS and gingivitis (n = 35); 3) systemically and periodontally healthy women (n = 25); and 4) systemically healthy women with gingivitis (n = 20). Enzyme-linked immunosorbent assay was used to determine levels of these biomarkers. A full-mouth clinical periodontal evaluation was performed for each patient. RESULTS: Salivary MMP-9 and NE levels, as well as MMP-9/TIMP-1 ratios, were higher in the systemically healthy women with gingivitis compared with periodontally healthy women with PCOS (P <0.001; P <0.01; and P <0.0001, respectively). Serum MMP-9 and MPO levels were higher in women with PCOS and gingivitis compared with periodontally healthy women with PCOS (P <0.05). Serum MMP-9 levels were lower in healthy women with gingivitis than systemically and periodontally healthy women or women with PCOS and gingivitis (P <0.05). PCOS groups exhibited a positive correlation among clinical periodontal parameters and serum MMP-9 levels or salivary MPO, NE levels, and MMP-9/MMP-1 ratio. Correlation was negative among clinical periodontal parameters and serum MMP-9 levels and MMP-9/TIMP-1 ratio in systemically healthy patients (P <0.05). CONCLUSIONS: The present findings emphasize that PCOS and gingival inflammation are associated with each other, as evidenced by salivary and serum levels of neutrophilic enzymes. This interaction may contribute to the perturbation of ovarian remodeling in PCOS.

Inflammatory mediator polymorphisms associate with initial periodontitis in adolescents.

Several studies have addressed cytokine gene polymorphisms and their possible associations with periodontitis. We examined the association between salivary anti- and pro-inflammatory mediator polymorphisms and initial periodontitis in Finnish adolescents, taking into account the effect of smoking. Salivary samples of 93 clinically examined adolescents from Eastern Finland were analyzed. Their oral health and smoking habits were recorded. Periodontal probing depth (PPD), and bleeding on probing (BOP) at four sites per tooth, root calculus (RC), and visible plaque index (VPI) were recorded from the index teeth. Salivary MMP-8 median values were assessed. The sites with ≥4 mm PD were categorized as follows: PPD1 = one or more ≥4 mm pocket, PPD2 = two or more ≥4 mm pockets, and PPD3 = three or more ≥4 mm pockets. Genomic DNA was extracted from 300 µl of the saliva samples by genomic QIAamp® DNA Blood Mini Kit and genotyped for polymorphisms. Genetic variants for genotyping were selected from the following genes of interest: S100A8, FCGR2A, FCGR2B, IL10, MMP8, MMP3, MMP13, VDR, TLR4, MMP2, MPO, ELANE, IL1A, IL1B, IL1RN, CD28, MMP9, DDX39B, NFKBIL1, LTA, TNF, SOD2, IL6, TLR4, TIMP1, and SYN1. After false discovery rate control (FDR), polymorphisms in MMP3 (rs679620, rs520540, rs639752), CD28 (rs3116496), and VDR (rs2228570) associated (FDR q < 0.05) with deepened periodontal pockets. Smoking did not affect the results. Genetic polymorphisms of pro-inflammatory mediators MMP3, CD28, and VDR seem to link to initial periodontitis.

Elevated matrix metalloproteinase-8 in saliva and serum in polycystic ovary syndrome and association with gingival inflammation.

This study aimed to investigate the levels of matrix metalloproteinase-8 (MMP-8) and tissue inhibitors of MMP-1 (TIMP-1) in saliva and serum samples of women with polycystic ovary syndrome (PCOS; n = 80) and matched systemically healthy controls (n = 45), with varying degrees of gingival inflammation. Salivary levels of MMP-8 and the MMP-8/TIMP-1 ratio were significantly elevated in women with PCOS, who also exhibited more gingivitis than systemically healthy women. No major changes were observed in salivary TIMP-1 levels with regard to PCOS. Serum levels of MMP-8 and the MMP-8/TIMP-1 ratio were significantly higher in women with PCOS, irrespective of the presence of gingivitis, while there were no differences in TIMP-1 levels. A positive correlation was indicated between probing depth, bleeding on probing, plaque index and salivary or serum MMP-8 levels or MMP-8/TIMP-1 ratio in the case of PCOS, while a negative such correlation was revealed for TIMP-1 in systemically healthy women. Increased levels of MMP-8 in saliva and serum seem to be more pronounced in women with PCOS, and potentiated in the presence of gingival inflammation. Alterations in MMP/TIMP system triggered by local and systemic inflammation may be implicated in the pathogenesis of PCOS, or the deterioration of its clinical presentation.