Is human giardiasis caused by two different Giardia species?

We have recently sequenced the genome of the human Giardia intestinalis assemblage B isolate GS.¹ Comparisons to the earlier sequenced genome of the human assemblage A isolate WB showed that the average amino acid identity in 4300 orthologous proteins was only 78%. Here we discuss these results in the light of new genome sequencing data from the hoofed-animal assemblage E (isolate P15, isolated from a pig) and further characterization of assemblage A and B isolates from humans. There is a highly conserved set of core genes (4557 genes, 91% of genome) common to all isolates. The largest genomic differences are found in variable, Giardia-specific gene families and a large number of chromosomal rearrangements were detected, even between different chromosomes. Surprisingly, the assemblage E and A isolates are more similar at the amino-acid level than the two human isolates are to each other. This strengthens our earlier data suggesting that humans are infected by two different species of Giardia.     

Is tracheal stenosis caused by percutaneous tracheostomy different from that by surgical tracheostomy?

STUDY OBJECTIVE: To compare the surgical findings of tracheal stenosis caused by percutaneous tracheostomy (PCT) and surgical tracheostomy (SGT). DESIGN AND SETTING: A combined prospective (from 2001 to 2003) and retrospective (from 1993 to 2001) observational study of the patients undergoing tracheal resection and reconstruction for treatment of tracheal stenosis following PCT or SGT in a national referral center for thoracic surgery in the United Kingdom. PATIENTS AND MEASUREMENTS: We studied 29 patients presenting with symptomatic tracheal stenosis requiring tracheal reconstruction. We recorded the demographic data, duration of mechanical ventilation, onset of tracheal stenosis after decannulation, and type of tracheostomy (PCT or SGT) from referral notes. Tracheal reconstruction was preceded by rigid bronchoscopy, through which the distance of the superior level of stenosis to the vocal cords, and the length and the diameter of stenosis were measured. The type of surgical technique for tracheal resection was also recorded. We then compared the stenosis caused by PCT (n = 15) and SGT (n = 14) using an unpaired t test, Mann-Whitney U test, or Fisher exact test as appropriate for statistical analysis. RESULTS: The mean distance from the superior level of stenosis in the PCT group was significantly closer to the vocal cords compared with the mean distance in the SGT group: 1.6 cm (95% confidence interval [CI], 1.1 to 2.1) vs 3.4 cm (95% CI, 2.3 to 4.5), respectively (p = 0.04). The mean onset of stenosis was significantly earlier in the PCT group compared to the SGT group: 5.0 weeks (95% CI, 5.0 to 6.0) vs 28.5 weeks (95% CI, 12 to 84), respectively (p = 0.009). Seven of 15 patients in the PCT group required partial cricoid resection and a mucosal flap, compared with 1 of 14 patients in the SGT group, although the difference did not reach statistic significance (p = 0.23). CONCLUSION: Stenosis caused by PCT occurred earlier and was subglottic in nature compared to that by SGT. Surgical correction of stenosis was more difficult in the PCT group due to its presentation in the subglottic area.     

Is this reaction caused by this drug?

The case report on cotrimoxazole-induced pancreatitis by Versleijen et al. deals with the assessment of the probability that cotrimoxazole induced the acute pancreatitis: a causality assessment. In this editorial, we comment on this assessment from a clinical, pharmacological and epidemiological perspective. Moreover, the consequences of the results of the assessment are discussed.     

Is chronic rhinosinusitis caused by persistent respiratory virus infection?

Background

Many chronic rhinosinusitis (CRS) patients recall an upper respiratory tract infection as the inciting event of their chronic illness. Viral infections have been shown to cause obstruction of the osteomeatal complex, which is likely to be a critical step in the development of CRS. There is clear overlap between the pathogenesis of CRS and asthma. Infections with respiratory viruses in childhood increase the risk of subsequently developing asthma. Viral infections in established asthmatics are associated with acute exacerbations. We sought to determine whether respiratory viruses could be detected within the sinonasal mucosa of CRS patients using polymerase chain reaction (PCR) techniques.

Methods

Sinus mucosa was sampled from 13 patients with CRS and 2 patients with normal sinuses. PCR was used to look for common respiratory viruses (parainfluenza 1, 2, and 3; respiratory syncytial virus [RSV]; human metapneumovirus [hMPV]; adenovirus [ADV]; rhinovirus; coronavirus; bocavirus [BoV]; cytomegalovirus [CMV]; and influenza A and B).

Results

No respiratory viruses were detected in any of the samples.

Conclusion

Persistence of respiratory viruses within the sinonasal mucosa is unlikely to be a cause of ongoing inflammation in CRS. The possibility remains that a transient viral infection provides the initial inflammatory stimulus. © 2011 ARS‐AAOA, LLC.

     

Is weaning failure caused by low-frequency fatigue of the diaphragm?

Because patients who fail a trial of weaning from mechanical ventilation experience a marked increase in respiratory load, we hypothesized that these patients develop diaphragmatic fatigue. Accordingly, we measured twitch transdiaphragmatic pressure using phrenic nerve stimulation in 11 weaning failure and 8 weaning success patients. Measurements were made before and 30 minutes after spontaneous breathing trials that lasted up to 60 minutes. Twitch transdiaphragmatic pressure was 8.9 +/- 2.2 cm H2O before the trials and 9.4 +/- 2.4 cm H2O after their completion in the weaning failure patients (p = 0.17); the corresponding values in the weaning success patients were 10.3 +/- 1.5 and 11.2 +/- 1.8 cm H2O (p = 0.18). Despite greater load (p = 0.04) and diaphragmatic effort (p = 0.01), the weaning failure patients did not develop low-frequency fatigue probably because of greater recruitment of rib cage and expiratory muscles (p = 0.004) and because clinical signs of distress mandating the reinstitution of mechanical ventilation arose before the development of fatigue. Twitch pressure revealed considerable diaphragmatic weakness in many weaning failure patients. In conclusion, in contrast to our hypothesis, weaning failure was not accompanied by low-frequency fatigue of the diaphragm, although many weaning failure patients displayed diaphragmatic weakness.     

Acute pancreatitis caused by leptospirosis： Report of two cases

Two cases of acute pancreatitis with leptospirosis are reported in this article. Case 1: A 68-year-old woman, presented initially with abdominal pain, nausea, vomiting, and jaundice. She was in poor general condition, and had acute abdominal signs and symptoms on physical examination. Emergency laparotomy was performed, acute pancreatitis and leptospirosis were diagnosed on the basis of surgical findings and serological tests. The patient died on postoperative d 6. Case 2: A 62-year-old man, presented with fever, jaundice, nausea, vomiting, and malaise. Acute pancreatitis associated with leptospirosis was diagnosed, according to abdominal CT scanning and serological tests. The patient recovered fully with antibiotic treatment and nutritional support within 19 d.     

Is insulin resistance caused by defects in insulin's target cells or by a stressed mind?

The importance of understanding insulin action is emphasized by the increasing prevalence of insulin resistance in various populations and by the fact that it plays an important pathophysiological role in many common disorders, for example, diabetes, obesity, hypertension and dyslipidemia. The primary factors responsible for the development of insulin resistance are so far unknown, although both genetic and environmental factors are involved. The genetic defects responsible for the common forms of insulin resistance, for example, in type 2 diabetes, are largely unidentified. Some studies from our group as well as by other investigators suggest that cellular insulin resistance is reversible and that it may be secondary to factors in the in vivo environment. These may include insulin-antagonistic action of hormones like catecholamines, glucocorticoids, sex steroids and adipokines as well as dysregulation of autonomic nervous activity and they could contribute to the early development of insulin resistance. Some of these factors can directly impair glucose uptake capacity and this might be due to alterations in key proteins involved in insulin's intracellular signaling pathways. This article briefly summarizes proposed mechanisms behind cellular and whole-body insulin resistance. In particular, we question the role of intrinsic defects in insulin's target cells as primary mechanisms in the development of insulin resistance in type 2 diabetes and we suggest that metabolic and neurohormonal factors instead are the main culprits.