Efficacy of the Treatment of Plantar Warts Using 1064 nm Laser and Cooling.

Cutaneous plantar warts may be treated using several optional methods, with the use of laser surgery having increased in the last few years. This work examined the efficacy of laser treatment combined with simple cooling to reduce pain. The cure rate was approximately 84%. There were no significant differences in the efficacy of treatment for different viral genotypes. The laser parameters were 500 msec pulses, 30 W of power, and a fluence of 212 J/cm2 delivered in up to four sessions. Successful treatment was achieved after an average of 3.6 sessions.

Human papillomaviruses genotyping in plantar warts.

Plantar warts are caused by human papillomaviruses (HPVs) and have been associated with several HPV genotypes. However, there are few studies focused exclusively on plantar warts. In this work, we aim to identify the HPV genotypes of plantar warts and explore their relation to demographic and clinical characteristics of patients. A total of 72 patients diagnosed with plantar warts were recruited at the Laser unit at Podiatric Hospital, University of Barcelona, Spain. Inner hyperkeratosis laminar sections of warts were collected and DNA of samples were extracted. Amplification of a conserved region of the HPV L1 gene was performed with the SK-Polymerase chain reaction method. DNA amplicons were sequenced and HPV types identified. The most prevalent genotypes detected among the 105 analyzed plantar warts were HPV-57 (37.1%), HPV-27 (23.8%), HPV-1a (20.9%), HPV-2 (15.2%), and HPV-65 (2.8%). The majority of patients (78%) presented one single plantar wart, whereas multiple warts were detected in 22.2% of patients. One patient with multiple warts presented HPV types from two different genera, suggesting the spread of warts by self-inoculation as well as by de novo infection. No significant differences between the number of warts in toes, midfoot and heel were found. The most prevalent HPV types detected in all areas belonged to the alpha genus. This work provides new insight on plantar warts and their associated HPV genotypes, and evidences the usefulness and reliability of both the sample collection procedure and the PCR method used for HPV detection and typing. J. Med. Virol. 89:902-907, 2017. © 2016 Wiley Periodicals, Inc.

Oral Microbiota, Periodontal Status, and Osteoporosis in Postmenopausal Females.

BACKGROUND: Alterations in hormone levels during menopause decrease bone density and may worsen oral health, favoring the growth of periodontal pathogens, whose detection could improve the diagnosis of periodontitis. The aim of this study is to detect and quantify the main periodontal pathogens in the oral microbiota of postmenopausal females and to explore the relationship between clinical and periodontal parameters. METHODS: This was an observational cross-sectional study of 76 postmenopausal females. Dental examinations and sampling for microbiologic evaluation were performed, and a history of osteoporosis/osteopenia was collected. Real-time polymerase chain reaction was used for detecting and quantifying Fusobacterium nucleatum (Fn), Aggregatibacter actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), Campylobacter rectus (Cr), and Tannerella forsythia (Tf). The results obtained were subjected to statistical analyses. Statistical significance was defined as P <0.05. RESULTS: Periodontitis was detected in 77.1% of females with osteoporosis/osteopenia (P >0.05). A significant correlation was found between osteoporosis and missing teeth. T. forsythia and C. rectus were detected in 100% of the samples, Fn and Pg in 98.7%, and Aa in 73.7%. CONCLUSIONS: Osteoporosis did not influence the prevalence of periodontitis among postmenopausal females. The presence of periodontopathogenic bacteria was not sufficient to confirm disease. A preventive maintenance program for postmenopausal females, particularly osteoporotic females, who are at greater risk of tooth loss, could minimize the potential effects of bone loss on periodontal tissues.

Interactions of the TnaC nascent peptide with rRNA in the exit tunnel enable the ribosome to respond to free tryptophan.

A transcriptional attenuation mechanism regulates expression of the bacterial tnaCAB operon. This mechanism requires ribosomal arrest induced by the regulatory nascent TnaC peptide in response to free L-tryptophan (L-Trp). In this study we demonstrate, using genetic and biochemical analyses, that in Escherichia coli, TnaC residue I19 and 23S rRNA nucleotide A2058 are essential for the ribosome's ability to sense free L-Trp. We show that the mutational change A2058U in 23S rRNA reduces the concentration dependence of L-Trp-mediated tna operon induction, whereas the TnaC I19L change suppresses this phenotype, restoring the sensitivity of the translating A2058U mutant ribosome to free L-Trp. These findings suggest that interactions between TnaC residue I19 and 23S rRNA nucleotide A2058 contribute to the creation of a regulatory L-Trp binding site within the translating ribosome.

The contribution of efflux pumps to quinolone resistance in Streptococcus pneumoniae clinical isolates.

Active efflux has been involved in fluoroquinolone resistance in Streptococcus pneumoniae. While only one efflux machinery has been well described (PmrA), the eventual existence of other pumps than PmrA has been suggested. The actual role of active quinolone efflux in producing ciprofloxacin resistance was examined by means of several methods. Strains HUB 2375 and HUB 3073 are clinical isolates resistant to fluoroquinolones. Since no mutations in the quinolone resistance-determining regions of these strains were found, resistance to fluoroquinolones should be attributed only to efflux. Strain R6 was transformed by DNA from both HUB 2375 and HUB 3073. Selected transformants were chosen for knockout of pmrA genes by polymerase chain reaction ligation mutagenesis in order to study the actual role and the degree of involvement of PmrA in determining ciprofloxacin resistance. Results strongly supported the hypothesis that efflux pumps other than PmrA are involved in fluoroquinolone resistance in clinical strains of pneumococci.