Effectiveness of voice therapy in reflux-related voice disorders.

Gastroesophageal reflux (GER) with laryngopharyngeal reflux plays a significant role in voice disorders. A significant proportion of patients attending ear, nose, and throat clinics with voice disorders may have gastroesophageal reflux disease (GERD). There is no controlled study of the effect of voice therapy on GERD. We assessed the effect of voice therapy in patients with dysphonia and GERD. Thirty-two patients with dysphonia and GERD underwent indirect laryngoscopy and voice analysis. Esophageal and laryngeal symptoms were assessed using the reflux symptom index (RSI). At endoscopy, esophagitis was graded according to Los Angeles classification. Patients were randomized to receive either voice therapy and omeprazole (20 mg bid) (n=16, mean [SD] age 36.1 [9.6] y; 5 men; Gp A) or omeprazole alone (n=16, age 31.8 [11.7] y; 9 men; Gp B). During voice analysis, jitter, shimmer, harmonic-to-noise ratio (HNR) and normalized noise energy (NNE) were assessed using the Dr. Speech software (version 4 1998; Tigers DRS, Inc). Hoarseness and breathiness of voice were assessed using a perceptual rating scale of 0-3. Parameters were reassessed after 6 weeks, and analyzed using parametric or nonparametric tests as applicable. In Group A, 9 patients had Grade A, 3 had Grade B, and 1 had Grade C esophagitis; 3 had normal study. In Group B, 8 patients had Grade A, 2 had Grade B esophagitis, and 6 had normal study. Baseline findings: median RSI scores were comparable (Group A 20.0 [range 14-27], Group B 19.0 [15-24]). Median rating was 2.0 for hoarseness and breathiness for both groups. Values in Groups A and B for jitter 0.5 (0.6) versus 0.5 (0.8), shimmer 3.1 (2.5) versus 2.8 (2.0), HNR 23.0 (5.6) versus 23.1 (4.2), and NNE -7.3 (3.2) versus -7.2 (3.4) were similar. Post-therapy values for Groups A and B: RSI scores were 9.0 (5-13; P<0.01 as compared with baseline) and 13.0 (10-17; P<0.01), respectively. Ratings for hoarseness and breathiness were 0.5 (P<0.01) and 1.0 (P<0.01) and 2.0. Values for jitter were 0.2 (0.0; P=0.02) versus 0.4 (0.7), shimmer 1.3 (0.7; P<0.01) versus 2.3 (1.2), HNR 26.7 (2.3; P<0.01) versus 23.7 (3.2), and NNE -12.3 (3.0, P<0.01) versus -9.2 (3.4; P<0.01). Improvement in the voice therapy group was significantly better than in patients who received omeprazole alone. Dysphonia is a significant problem in GER. Treatment for GER improves dysphonia, but in addition, voice therapy enhances the improvement.

Microsomal chitinase activity from Candida albicans.

Chitinase (E.C. 3.2.1.14) was characterized in microsomal fractions from yeast cells of Candida albicans. Following six washes with buffer (50 mM Bis-Tris.Cl, pH 6.5), enzyme activity of microsomes fell markedly to 0.3% of total and 6% of the specific activity detected in the low-speed supernatant (9000 X g) of a cell lysate. An apparently zymogenic, microsomal chitinase activity became more readily detectable with washing and after six washes enzyme activity was activated 1.7-fold following pre-incubation with trypsin. The following properties of microsomal chitinase were closely comparable with those for cytosolic chitinase (indicated in parentheses): Km = 2.1 mg chitin per ml (2.9 mg chitin per ml); temperature optimum = 45 degrees C (45 degrees C); inhibition by allosamidin competitive, Ki = 0.29 microM (competitive, Ki = 0.23 microM). A range of detergents solubilized and activated microsomal chitinase in a highly specific manner. Following density gradient centrifugation of microsomes, chitinase was distributed approximately evenly throughout the gradient suggesting that microsomal chitinase is not associated exclusively with any one membrane component. The possible morphogenetic role of microsomal chitinase is discussed in relation to the potential of this enzyme as a target for highly specific antifungal agents.

Role of environmental cleaning in controlling an outbreak of Acinetobacter baumannii on a neurosurgical intensive care unit.

An outbreak of Acinetobacter baumannii colonization and infection occurred in 19 patients over a 14-month period during 1998-1999 on a neurosurgical intensive care unit. During efforts to control the outbreak a significant correlation was observed between the number of environmental isolates of A. baumannii obtained during each monthly screening and the number of patients with A. baumannii colonization/infection in the same calendar month (P=0.004). Use of 1000 ppm hypochlorite solution and the introduction of new cleaning protocols reduced the number of environmental isolates. Failure to maintain low levels of environmental contamination with A. baumannii resulted in increases in patient colonization. This study showed that high standards of cleaning play an integral role in controlling outbreaks of A. baumannii in the intensive care unit setting.

Rapid spread of penicillin-resistant Streptococcus pneumoniae among high-risk hospital inpatients and the role of molecular typing in outbreak confirmation.

This study describes an outbreak of penicillin-resistant Streptococcus pneumoniae among patients on an ear, nose and throat (ENT) ward. Over a period of 10 days, S. pneumoniae [penicillin minimum inhibitory concentration (MIC) 0.75] was isolated from a total of seven patients with symptoms and signs of lower respiratory tract infection. Standard source isolation was implemented and the ward was closed to admissions and discharges. Screening of nasopharyngeal secretions was undertaken on all patients and staff contacts. Three patients (of eight possible contacts) and none of the staff (47 screened) were identified as colonized with the same strain. Nasal mupirocin and oral rifampicin were administered to carriers. Confirmation of the outbreak was achieved rapidly using a contemporary molecular typing method (pulsed-field gel electrophoresis) and timely introduction of infection control measures successfully contained the outbreak. Implications for pneumococcal vaccination are discussed.

Ventilation grilles as a potential source of methicillin-resistant Staphylococcus aureus causing an outbreak in an orthopaedic ward at a district general hospital.

The spread of methicillin-resistant Staphylococcus aureus (MRSA) in a hospital is thought to be mainly by direct contact. Environmental sources such as exhaust ducting systems have been increasingly recognized as a source for MRSA outbreaks in intensive therapy units. We describe an outbreak of MRSA related to ventilation grilles in an orthopaedic ward. Six patients and one nurse were involved in an outbreak with EMRSA-15 during March 1996. The index case was transferred from a large university hospital in Leeds. One of the patients had shared the same bay with the index case. The rest of the patients were in another bay of the same ward and had no direct contact with the index patient. An environmental source was suspected and the ventilation grilles in boys 1 and 2 were found to be harbouring EMRSA-15. The ventilation system at that time was working on an intermittent cycle from 4 p.m.-8 a.m. Daily shut-down of the system temporarily created a negative pressure, sucking air in from the ward environment into the ventilation system and probably contaminating the outlet grilles. It is likely that contaminated air was blown back into the ward when the ventilation system was started. The system was thoroughly cleaned, appropriate infection control measures were instituted and the ventilation system was put back on a continuous running cycle and the outbreak terminated. Six months after the outbreak no isolates of EMRSA-15 had been made on the ward.

Stenotrophomonas maltophilia contamination of nebulizers used to deliver aerosolized therapy to inpatients with cystic fibrosis.

There is circumstantial evidence that nebulizer equipment may be a source of Stenotrophomonas maltophilia for patients with cystic fibrosis. Eighty-nine inpatient nebulizers were examined for evidence of S. maltophilia contamination of which nine (10%) yielded 14 strains of the bacterium. Environmental samples were obtained from 73 different sites on the ward, of which 17 (23%) yielded a further 21 strains. Positive sites included taps, sink drains, and potable water. Genotyping using ERIC-PCR and pulsed-field gel electrophoresis revealed that two pairs of patients' nebulizers were contaminated with closely related strains. None of the S. maltophilia isolates obtained from the ward environment shared genotypes with those obtained from the nebulizers. The frequency of isolation of S. maltophilia from potable water sources on the ward suggests that contamination may result from using it to clean reusable nebulizer equipment, particularly if this is followed by inadequate drying. Although the actual source of S. maltophilia contamination of hospital-use nebulizer equipment in this study remained elusive, these results have important infection control implications.

Role of environmental cleaning in controlling an outbreak of Acinetobacter baumannii on a neurosurgical intensive care unit.

An outbreak of Acinetobacter baumannii colonization and infection occurred in 19 patients over a 14-month period during 1998-1999 on a neurosurgical intensive care unit. During efforts to control the outbreak a significant correlation was observed between the number of environmental isolates of A. baumannii obtained during each monthly screening and the number of patients with A. baumannii colonization/infection in the same calendar month (P < 0.004). Use of 1000 ppm hypochlorite solution and the introduction of new cleaning protocols reduced the number of environmental isolates. Failure to maintain low levels of environmental contamination with A. baumannii resulted in increases in patient colonization. This study showed that high standards of cleaning play an integral role in controlling outbreaks of A. baumannii in the intensive care unit setting.

Transmission of colistin-resistant Pseudomonas aeruginosa between patients attending a pediatric cystic fibrosis center.

We report on an outbreak of colistin-resistant Pseudomonas aeruginosa (CRPA) that occurred in a United Kingdom pediatric cystic fibrosis (CF) unit and involved six children over a period of 5 years. All CRPA-positive children had received aerosolized colistin therapy before first isolation of resistant organisms (mean duration, 3.1 years). Four of the 6 had also received courses of intravenous colistin in the year before the first isolation of CRPA. No impact of CRPA acquisition on respiratory function, clinical condition, or radiological parameters could be demonstrated. Four of the 6 children carried isolates of CRPA indistinguishable on genotyping. Two of these 4 children were sisters. The other 2 were on the same ward together at time of first isolation, and subsequently shared overlapping admissions with one of the sisters. While there is no conclusive evidence for the route of transmission, the frequency of overlapping in-patient admissions between 3 of these patients is suggestive of patient-to-patient transfer in the nosocomial setting.CF clinicians should be aware that colistin resistance can occur in P. aeruginosa, and some of these strains are capable of spread within CF units.

Correlation between genotype and beta-lactamases of clinical and environmental strains of Stenotrophomonas maltophilia.

Heterogeneity of beta-lactamase production by 17 clinical and nine environmental isolates of Stenotrophomonas maltophilia was investigated using MICs of six different beta-lactam antibiotics, isoelectric focusing (IEF) and pulsed field gel electrophoresis. There was no clear correlation between the results of IEF, genotype and MIC determination. Environmental isolates were more susceptible than clinical isolates; eight clinical and none of the environmental isolates expressed high-level resistance to meropenem. Only two isolates expressed high-level resistance to ceftazidime. These results indicate that further studies are required to elucidate the extent of genetic heterogeneity within the L1 and L2 beta-lactamase genes.

Chitinase activity from Candida albicans and its inhibition by allosamidin.

Candida albicans chitinase isolated using the Dyno-Mill disruption technique was characterized using an improved radiometric assay procedure. The enzyme had apparent temperature and pH optima of 45 degrees C and 6.5, respectively. The preparation yielded an apparent Km of 3.9 mg chitin ml-1 [17.6 mM-N-acetylglucosamine (GlcNAc) equivalents] and V of 2.3 nmol GlcNAc formed min-1 (mg protein)-1. The potential of the streptomycete antibiotic allosamidin as an antifungal agent is discussed in view of its dose-dependent inhibition of C. albicans chitinase activity (IC50 = 0.3 microM). Allosamidin was a potent competitive inhibitor of enzyme activity (Ki = 0.23 microM).

Comparison and application of ribosome spacer DNA amplicon polymorphisms and pulsed-field gel electrophoresis for differentiation of methicillin-resistant Staphylococcus aureus strains.

Analysis of sequences in the fragments of the 16S-23S rRNA intergenic spacer region by the ribosome spacer PCR (RS-PCR) can differentiate strains of methicillin-resistant Staphylococcus aureus (MRSA). We compared this technique with pulsed-field gel electrophoresis (PFGE) for typing MRSA strains and its application during an investigation of an outbreak. A total of 180 isolates of MRSA collected from various hospital laboratories within the United Kingdom and elsewhere were typed by PFGE and RS-PCR. PFGE identified 17 different types among the 180 strains examined, and RS-PCR generated 13 different types. PFGE could detect minor genetic variations among the isolates and could identify the variants which were not discriminated by RS-PCR. Four unique strain types detected by PFGE were not detected by RS-PCR. When applied to typing the outbreak-related strains from the vascular surgery unit at the General Infirmary at Leeds, the results of RS-PCR were identical to those of PFGE. Our results have shown that RS-PCR is a rapid, inexpensive technique that is highly reproducible and almost as discriminatory as PFGE for typing MRSA isolates and should be useful in the local investigation of MRSA outbreaks.