Phospholipase activity of Candida albicans isolates from patients with denture stomatitis: the influence of chlorhexidine gluconate on phospholipase production

BACKGROUND AND OBJECTIVES: The extracellular phospholipases of Candida albicans are considered to play a significant role in the pathogenesis of human infections. Therefore 23 clinical oral isolates of C. albicans from patients with denture stomatitis and 22 commensal oral isolates obtained from the palatal mucosa of healthy subjects were assayed for phospholipase activity. It is generally accepted that chlorhexidine gluconate is an appropriate adjunct or an alternative to antimycotic therapy in the management of oral candidiasis. However, the intraoral concentrations of this antiseptic fluctuate considerably due to the dynamics of the oral cavity. So the second main objective of this study was to investigate the effect of brief exposure (30 min) to two sub-therapeutic concentrations (0.002% and 0.0012%) of chlorhexidine gluconate on the value of phospholipase production (Pz) of C. albicans. METHOD: An in vitro phospholipase production was done by plate assay method using an egg yolk-agar medium. RESULTS: No significant differences were found in the number of C. albicans isolates producing phospholipase between two groups. However, the mean value of Pz produced by the isolates from patients with denture stomatitis was significantly (p<0.05) higher than the commensals. Exposure of the isolates to 0.002% and 0.0012% chlorhexidine led to a significant (p<0.001 and p<0.01, respectively) reduction in the amount of phospholipase. CONCLUSION: The results of this study imply that sub-therapeutic levels of chlorhexidine may modulate candidal phospholipase activity, thereby suppressing pathogenicity of C. albicans.     

Impact of perioperative acute ischemic stroke on the outcomes of noncardiac and nonvascular surgery: a single centre prospective study

Background

Although ischemic stroke is a well-known complication of cardiovascular surgery it has not been extensively studied in patients undergoing noncardiac surgery. The aim of this study was to assess the predictors and outcomes of perioperative acute ischemic stroke (PAIS) in patients undergoing noncardiothoracic, nonvascular surgery (NCS).

Methods

We prospectively evaluated patients undergoing NCS and enrolled patients older than 18 years who underwent an elective, non-daytime, open surgical procedure. Electrocardiography and cardiac biomarkers were obtained 1 day before surgery, and on postoperative days 1, 3 and 7.

Results

Of the 1340 patients undergoing NCS, 31 (2.3%) experienced PAIS. Only age (odds ratio [OR] 2.5, 95% confidence interval [CI] 1.01–3.2, p < 0.001) and preoperative history of stroke (OR 3.6, 95% CI 1.2–4.8, p < 0.001) were independent predictors of PAIS according to multivariate analysis. Patients with PAIS had more cardiovascular (51.6% v. 10.6%, p < 0.001) and noncardiovascular complications (67.7% v. 28.3%, p < 0.001). In-hospital mortality was 19.3% for the PAIS group and 1% for those without PAIS (p < 0.001).

Conclusion

Age and preoperative history of stroke were strong risk factors for PAIS in patients undergoing NCS. Patients with PAIS carry an elevated risk of perioperative morbidity and mortality.     

Calcaneal Avulsion of an Ochronotic Achilles Tendon: A Case Report

Alkaptonuria is a hereditary disorder of phenylalanine and tyrosine, with an incidence of approximately 1/200,000 to 1/1,000,000. Ochronosis is the accumulation of homogentisic acid and its metabolites in connective tissues such as the tendons, cartilage, and skin. In the present case study, a 50-year-old male presented with a nontraumatic calcaneal avulsion without a previous diagnosis of ochronosis. To the best of our knowledge, little information has been reported of this pathology in the Achilles tendon and the surgical management.     

A novel homozygous SLC25A1 mutation with impaired mitochondrial complex V: Possible phenotypic expansion

SLC25A1 mutations are associated with combined D,L‐2‐hydroxyglutaric aciduria (DL‐ 2HGA; OMIM #615182), characterized by muscular hypotonia, severe neurodevelopmental dysfunction and intractable seizures. SLC25A1 encodes the mitochondrial citrate carrier (CIC), which mediates efflux of the mitochondrial tricarboxylic acid (TCA) cycle intermediates citrate and isocitrate in exchange for cytosolic malate. Only a single family with an SLC25A1 mutation has been described in which mitochondrial respiratory chain dysfunction was documented, specifically in complex IV. Five infants of two consanguineous Bedouin families of the same tribe presented with small head circumference and neonatal‐onset encephalopathy with severe muscular weakness, intractable seizures, respiratory distress, and lack of psychomotor development culminating in early death. Ventricular septal defects (VSD) were demonstrated in three patients. Blood and CSF lactate were elevated with normal levels of plasma amino acids and free carnitine and increased 2‐OH‐glutaric acid urinary exertion. EEG was compatible with white matter disorder. Brain MRI revealed ventriculomegaly, thin corpus callosum with increased lactate peak on spectroscopy. Mitochondrial complex V deficiency was demonstrated in skeletal muscle biopsy of one infant. Homozygosity mapping and sequencing ruled out homozygosity of affected individuals in all known complex V‐associated genes. Whole exome sequencing identified a novel homozygous SLC25A1 c.713A>G (p.Asn238Ser) mutation, segregating as expected in the affected kindred and not found in 220 control alleles. Thus, SLC25A1 mutations might be associated with mitochondrial complex V deficiency and should be considered in the differential diagnosis of mitochondrial respiratory chain defects.

     

Coronary artery thromboembolism: Unexpected presentation of left atrial myxoma covered with thrombus

Cardiac myxomas are benign primer cardiac tumors of the heart. They can be fatal with a thromboembolic presentation. Myocardial infarction is one of these unusual thromboembolic presentations. We report a patient who presented with cardiac arrest due to ventricular fibrillation related to myocardial infarction. After successful resuscitation, coronary angiography and transthoracic echocardiography were performed. A left atrial mass was observed and interpreted as a possible cause of coronary embolism leading to myocardial infarction. After surgical excision, the pathological examination confirmed myxoma, which was the essential cause of the tendency to arterial embolism.     

COVID-19 in solid organ transplant recipients: a single-center experience

Solid organ transplant (SOT) recipients may be at risk for severe COVID-19. Data on the clinical course of COVID-19 in immunosuppressed patients are limited, and the effective treatment strategy for these patients is unknown. We describe our institutional experience with COVID-19 in SOT. Demographic, clinical, and treatment data were extracted from the electronic patient files. A total of 23 SOT transplant recipients suffering from COVID-19 were identified (n = 3 heart; n = 15 kidney; n = 1 kidney-after-heart; n = 3 lung, and n = 1 liver transplant recipient). The presenting symptoms were similar to nonimmunocompromised patients. Eighty-three percent (19/23) of the patients required hospitalization, but only two of these were transferred to the intensive care unit. Five patients died from COVID-19; all had high Clinical Frailty Scores. In four of these patients, mechanical ventilation was deemed futile. In 57% of patients, the immunosuppressive therapy was not changed and only three patients were treated with chloroquine. Most patients recovered without experimental antiviral therapy. Modification of the immunosuppressive regimen alone could be a therapeutic option for SOT recipients suffering from moderate to severe COVID-19. Pre-existent frailty is associated with death from COVID-19.