The impact of intraoperative saline irrigations on bacterial load within the maxillary sinus.

BACKGROUND: Saline irrigations are routinely employed during endoscopic sinus surgery to remove mucous and debris from the sinus cavities. What is unknown is whether this results in a quantitative reduction in pathologic bacteria within the sinus mucosa. The objectives of this study were to quantify the amount of 5 different bacteria (Staphylococcus aureus, Haemophilus influenzae, Pseudomonas aeruginosa, coagulase-negative Staphylococcus (CNS), and Streptococcus pneumoniae) within the maxillary sinus and to determine the impact of saline irrigations on bacterial counts. METHODS: Twenty patients with chronic rhinosinusitis were prospectively enrolled. After bilateral maxillary antrostomies, biopsies were taken of the maxillary sinus mucosa prior to any irrigation. In each patient, the left maxillary sinus was then irrigated with 250 cc of normal saline (NS) with a pressurized pulse-irrigation device and the right side was irrigated with 250 cc of NS using a 30-cc syringe attached to a curved suction tip. Repeat maxillary sinus mucosal biopsies were then taken from each side. Each biopsy was analyzed using quantitative polymerase chain reaction to determine the presence and amount of each of the bacteria. RESULTS: Saline irrigations were found to significantly reduce the amount of S. aureus, P. aeruginosa, and S. pneumoniae found within the maxillary sinus mucosa. No difference was found for H. influenzae or CNS. No difference in bacterial load reduction was able to be shown between the pressurized saline flushes and manual saline rinse methods. CONCLUSION: Intraoperative saline irrigations are able to significantly reduce the amount of potentially pathogenic bacteria within the diseased sinus mucosa.

Genome-wide screening for genetic loci associated with noise-induced hearing loss.

Noise-induced hearing loss (NIHL) is one of the more common sources of environmentally induced hearing loss in adults. In a mouse model, Castaneous (CAST/Ei) is an inbred strain that is resistant to NIHL, while the C57BL/6J strain is susceptible. We have used the genome-tagged mice (GTM) library of congenic strains, carrying defined segments of the CAST/Ei genome introgressed onto the C57BL/6J background, to search for loci modifying the noise-induced damage seen in the C57BL/6J strain. NIHL was induced by exposing 6-8-week old mice to 108 dB SPL intensity noise. We tested the hearing of each mouse strain up to 23 days after noise exposure using auditory brainstem response (ABR). This study identifies a number of genetic loci that modify the initial response to damaging noise, as well as long-term recovery. The data suggest that multiple alleles within the CAST/Ei genome modify the pathogenesis of NIHL and that screening congenic libraries for loci that underlie traits of interest can be easily carried out in a high-throughput fashion.

Genetics of hearing loss: Allelism and modifier genes produce a phenotypic continuum.

Recent genetic and genomic studies have greatly advanced our knowledge of the structure and function of genes involved in hearing loss. We are starting to recognize, however, that many of these genes do not appear to follow traditional Mendelian expression patterns and are subject to the effects of allelism and modifier genes. This review presents two genes illustrative of this concept that have varied expression pattern such that they may produce either syndromic or nonsyndromic hearing loss. One of these genes, cadherin 23, produces a spectrum of phenotypic traits, including presbycusis, nonsyndromic prelingual hearing loss (DFNB12), and syndromic hearing loss as part of Usher syndrome (Usher 1D). Missense mutations in CDH23 have been associated with presbycusis and DFNB12, whereas null alleles cause the majority of Usher 1D. Modifier gene products that interact with cadherin 23 also affect the phenotypic spectrum. Similarly, allelsim in the gene encoding wolframin (WFS1) causes either a nonsyndromic dominant low-frequency hearing loss (DFNA6/14/38) or Wolfram syndrome. Missense mutations within a defined region are associated with DFNA6/14/38, while more severe mutations spanning WFS1 are found in Wolfram syndrome patients. The phenotypic spectrum of Wolfram syndrome is also hypothesized to be influenced by modifier genes products. These studies provide increasing evidence for the importance of modifier genes in elucidating the functional pathways of primary hearing loss genes. Characterizing modifier genes may result in better treatment options for patients with hearing loss and define new diagnostic and therapeutic targets.