Trench fever is caused by Bartonella (Rochalimaea) quintana, a small gram-negative rod that is transmitted by body lice. Recently, B. quintana infections in homeless patients have been reported in the United States and Europe. From October 1993 to October 1994, the seroprevalence of antibodies to B. quintana was assessed by indirect immunofluorescence in a prospective study of 221 nonhospitalized homeless people, 43 hospitalized homeless patients (cases), 250 blood donors, and 57 hospitalized matched controls. Four (1.8%) of 221 nonhospitalized homeless people tested had titers of > 1:100. Of the 43 cases, seven (16%) had serological titers of > or = 1:100. None of the 250 serum samples from blood donors contained antibodies to B. quintana. The presence of antibodies to B. quintana in cases was significantly associated with the presence of body lice, exposure to cats, headaches, eastern European origin, and pain in the legs. This study demonstrates the presence of antibodies to B. quintana in the homeless population and should alert physicians that B. quintana might be an etiologic agent of fever in homeless patients.

Background: The ‘case-crossover’ design is a strategy fitted to studying transient effects of intermittent exposure on acute-onset disease occurring shortly after exposure. It has the important advantage of eliminating most confounding variables, allowing a stronger causality inference. Objectives: The objective of the study was to evaluate the relationships between emergency room (ER) visits for asthma attacks and gaseous air pollution changes. Methods: The study included 549 individuals, 3–49 years old, visiting the ER during 1 year. Exposure to gaseous air pollutants (SO₂, NO₂, O₃) on the same day and up to 4 days before was computed according to the patient’s address. The statistical analysis included meteorological data as potential confounding variables. Results: No association could be shown between ER visits and SO₂ or NO₂ levels. In contrast, there was a statistically significant association between ER visits and mean O₃ levels, on the day of admission and also on D –2 and D –3. For an increase of 10 µg/m³, the risk of requiring an ER admission increased by 6–10%. Conclusions: Using this new strategy, we confirmed that ozone changes lead to a moderate increase in risk of requiring an ER admission in asthmatic subjects.

Data on tolerance of cardiac pacemakers during diving are very scarce. The aim of this study was to test electronic and mechanical tolerances of pacemakers exposed to experimental reproductions of pressures encountered during diving. Two samples each of 20 different models of cardiac pacemakers were exposed to compression during continuous telemetric monitoring. The first sample of each model was exposed to a pressure of 60 metres of sea water (msw). Each second sample was first exposed to a pressure of 30 msw then to 60 msw hyperbaric testing, with a period of 1 month between the two tests. Electronic function and structural integrity of the cans were evaluated. No electronic dysfunction was noted. We merely observed in some devices a transient increase of the pacing rate during pressurisation. No significant deformation of the can (< or =0.2 mm) was observed after the 30 msw hyperbaric test. However, after the 60 msw test, more than half of the devices tested were significantly and definitively deformed. These results show that tested pacemakers preserved a normal electronic function up to 60 msw but most of the tested devices demonstrated significant deformations of the pacemaker can for the hyperbaric exposure observed deeper than 30 msw. Without prejudging diving aptitude for implanted pacemaker patients, it therefore seems prudent to advise them against diving beyond 30 msw because of the potential for electronic dysfunction beyond that depth.

No abstract

Positive pressure breathing produced by mechanical ventilation with an expiratory threshold load (ETL) may modify electrocardiogram (ECG) complexes independently of any recording artefact due to lung volume changes. Anaesthetized, paralyzed rabbits were treated for about 2 h, then killed. In intact then vagotomized animals two situations were studied successively. Firstly, positive inspiratory pressure breathing, and secondly, positive inspiratory plus expiratory pressure breathing by adding ETL to mechanical ventilation. Arterial blood gases were measured and held constant throughout the challenge. Oesophageal pressure, giving indirect measurement of intrathoracic pressure, arterial blood pressure, blood flows in abdominal aorta and inferior vena cava and standard ECG recordings were made at baseline condition during mechanical ventilation, then at the end of a 10-min period of ETL breathing. The ETL breathing decreased arterial blood pressure significantly and reduced arterial and venous blood flows in the same proportion. No change in the duration of ECG complexes was noticed. However, ETL markedly reduced the amplitude of P- and T-waves, but not that of R-wave, an effect significantly accentuated after vagotomy. The ETL breathing increased the T-vector angle, with no associated change in QRS vector angle. The present animal investigations revealed that positive pressure breathing modifies the ECG independently of the consequences of ETL-induced lung volume changes. We speculate that the changes in P- and T-wave amplitude may have resulted from a reduced transmural pressure gradient between the epicardium and endocardium.