We examined 80 patients with acute obstructive anuria by ultrasound (US). Four of the 80 patients did not have dilatation of the urinary tract. In all four cases, antegrade pyelography guided by real-time US demonstrated urinary tract obstruction after the four patients had experienced 4, 5, 8, and 34 days of anuria, respectively. Diuresis occurred as a result of percutaneous nephrostomy in all four cases. Three of the patients were successfully treated by percutaneous techniques alone. Our findings demonstrate that even a complete and long-term obstruction of the urinary tract does not necessarily induce dilatation in the upper part of the tract. In such cases, only the direct opacification of the urinary tract can help confirm that the obstruction is present. Even in the absence of dilatation, antegrade pyelography guided by real-time US is a possible diagnostic method and can be the first step in the performance of percutaneous nephrostomy.

Question addressedIn contrast with pain, dyspnoea is not visible to the general public who lack the corresponding experiential baggage. We tested the hypotheses that the generalised use of face masks to fight SARS-CoV2 dissemination could change this and sensitise people to respiratory health.MethodsGeneral population polling (1012-person panel demographically representative of the adult French population –quota sampling method–; 517 women, 51%). 860 (85%) answered “no” to “treated for a chronic respiratory disease” (“respiratory healthy”, RH) and 152 “yes” (“respiratory disease”, RD). 14% of RH respondents reported having a close family member treated for a chronic respiratory disease (RH-family+ and RH-family−). Respondents described mask-related attitudes, beliefs, inconveniencies, dyspnoea, and changes in their respiratory health vision.ResultsCompliance with masks was high (94.7%). Dyspnoea ranked first among mask inconveniencies (RD 79.3%, RH 67.3%, p=0.013). “Air hunger” was the main sensory dyspnoea descriptor. Mask-related dyspnoea was independently associated with belonging to RH-family+ (Odds Ratio [OR] [95% confidence interval (CI)]: 1.85 [1.16–2.98]) and removing masks to improve breathing (OR 5.21 [3.73–7.28]). It was negatively associated with considering masks effective to protect others (OR]: 0.42 [0.25–0.75]). Half the respondents were more concerned with their respiratory health since wearing masks; 41% reported better understanding patients’ experiences.Answer to the questionWearing protective face masks leads to the mass discovery of breathing discomfort. It raises the public's awareness of what respiratory diseases involve and sensitises to the importance of breathing. These data should be used as the fulcrum of respiratory-health-oriented communication actions.

The primary pathogenetic mechanism responsible for the distinctive demyelinating lesions in the Central Nervous System (CNS) in Multiple Sclerosis (MS), first described in remarkable detail by Charcot more than 170 years ago, remains one of the most baffling conundrums in medicine. A possible role for bacterial cell molecules and transportable proteins in the pathogenesis of MS is reviewed. The ability of bacterial toxins to distort immunity and to cause distinctive toxic damage in the nervous system is discussed in the light of largely forgotten data linking bacterial nasopharyngeal infections with optic neuritis, optochiasmatic arachnoiditis and MS. While the blood-brain barrier substantially protects the CNS from hematogenous toxins, there is a route by which the barrier may be by-passed. Data is reviewed which shows that the CSF and extra-cellular fluid circulation is bi-directionally linked to the lymphatic drainage channels of the nasopharyngeal mucosa. While this provides a facility by which the CNS may mount immunological responses to antigenic challenges from within, it is also a route by which products of nasopharyngeal infection may drain into the CNS and be processed by the immune cells of the meninges and Virchow-Robin perivascular spaces. If potentially toxic bacterial products are identified in early MS tissues at these sites, this would provide an entirely new insight into the pathogenetic mechanisms of this frustratingly enigmatic disease.

Intensive care unit (ICU) patients are exposed to many sources of discomfort, among which dyspnoea is one of the more severely distressing [1]. In invasively mechanically ventilated patients, dyspnoea is frequent (47% of intubated patients report breathing discomfort when they can first communicate with caregivers) and severe (median rating of 5 on a dyspnoea visual analogue scale (D-VAS); association with anxiety and neurovegetative signs of stress) [2]. It is often linked to ventilator settings and seems to be associated with poorer clinical outcomes (e.g. delayed extubation and post-traumatic stress disorders) [2,3]. As in other settings, identifying and quantifying dyspnoea in mechanically ventilated patients is therefore a major clinical issue. This is challenging because self-report and self-assessment, prerequisites for D-VAS assessment [4], are often impossible or very difficult in this setting. Unfortunately, caregivers markedly underestimate dyspnoea in this context [5,6]. The risk of occult respiratory suffering is therefore major in the ICU setting and neglecting it would amount to medical error [7].

Highly significant clinical, epidemiological and pathogenetic similarities between multiple sclerosis (MS) and nasopharyngeal sinusitis has led to the hypothesis that MS is caused by the inadvertent incorporation of the lymphatic drainage of the nasopharynx into the extracellular fluid circulation of the CNS. It has been postulated that, in response to antigenic and toxic products generated by the mucosal nasopharygeal flora, the leptomeninges and CNS parenchyma acquire the characteristics of a persistently stimulated lymphoid organ. Using an extensive panel of bacterial antibodies, tissues from exceptionally early cases, identified and classified using multifactorial cluster analysis, were screened for bacterial antigens using immunohistological methods. Anti-staphylococcal antibodies detected antigen co-locating with IgG/C3d immune complexes in pre-demyelinating and in primary lesions. The distribution of the antigen in relation to the morphogenesis of early acute MS lesions is detailed. Evidence for the intrathecal processing of staphylococcal antigen was obtained using isoelectric focusing and antigen imprinting to identify antigen-specific oligoclonal bands. Employing a combination of isoelectric focusing, western blotting and mass spectrometric analysis, evidence for the intrathecal processing of staphylococcal β-haemolysin (sphingomyelinase) was obtained using CSF from MS cases. While a myelinolytic transportable toxin may be an important component in the pathogenesis of demyelination, in oligodendrocyte apoptosis, and in deviant immune responses within the CNS, the detection of other as yet unidentified staphylococcal-positive and negative oligoclonal bands points to the involvement of a cocktail of transportable antigens leaking in a similar manner into the CNS from the paranasal sinus mucosal tissues where these molecules are conserved by the resident flora to manipulate and subvert the normal processes of local and systemic immunity. Evidence for the access of other bacterial transportables to the CNS in MS should now be sought. The presence of 'high-output' toxigenic bacterial strains within the nasopharyngeal flora of MS patients should also be explored. The use of tracer molecules to detect and quantify nose-to-brain transport in MS patients is clearly apposite.

In a previous immunohistological study of tissues from unusually early cases of MS cluster analysis revealed a progression of demyelination through five distinct stages [Gay F, Drye T, Dick G, et al. The application of multifactorial cluster analysis in the staging of plaques in early multiple sclerosis. Identification and characterization of the primary demyelinating lesion. Brain 1997;120:1461-83]. Tissues from six of the earliest cases in this series contained regions of normal appearing white and grey matter in which well developed inflammatory events, concentrated in perivascular spaces, were found to extend locally into the perivascular parenchyma to envelop ostensibly intact myelin sheaths. The beginnings of myelin sheath lysis and phagocytosis were subsequently detected within these lesions and similar foci were found in subpial and in subependymal tissues. They were characterised by a spreading HLA Class II antigen expression on microglia, and by the presence of co-locating C3 complement-IgG complexes on capillary basement membranes, on microglial cell membranes and within the cytoplasm of large bodied activated astrocytes. Parenchymal lesions contained significantly few CD4+ T cells and showed no evidence of capillary leakage of plasma proteins. Despite the presence of complexed immunoglobulin and complement, opsonization of the myelin sheath could not be demonstrated. These observations point to the presence in early MS of a diffusing, complement-fixing, myelinolytic antigen, processed mainly within the Virchow-Robin spaces and distributed in the cerebrospinal and extracellular fluid compartments of the central nervous system.

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The lungs of conventional rats with chronic pneumonia contained Streptobacillus moniliformis and Mycoplasma pulmonis. These organisms singly and in combination failed to produce lung disease when inoculated into specific pathogen-free rats. On the other hand, diseased lung homogenate not containing cultivable organisms caused a chronic pneumonia when inoculated into specific pathogen-free rats. The organism involved was seen by electron microscopy and is morphologically indistinguishable from the grey lung agent of Andrewes and Glover and Nelson's enzootic bronchiectasis "virus." All of these agents have morphological and biological properties which indicate close relationship to the mycoplasmas. However, we failed to culture them either in tissue cultures or on inanimate media and conclude that a group of highly fastidious mycoplasma-like agents are a cause of chronic pneumonia in rodents. The preparation of reagents and techniques used in complement fixation tests were as described by Card (2). Transmission experiments in rats. To investigate the pathogenicity of lung homogenates and of or-83