[Outbreak of methicillin-resistant Staphylococcus aureus in general hospital intensive care unit]. / Epidémie à Staphylococcus aureus résistant à la méticilline dans une réanimation polyvalente d'un hôpital général.

Mantes' hospital polyvalent intensive care unit (ICU) experienced an outbreak episode caused by methicillin resistant Staphylococcus aureus (MRSA). Suspicion of physicians was strengthened by observing the weekly reading of multiresistant germs and the significative increase of MRSA carriers incidence rate, compared with the number of admission in the ICU: 5.5% to 11.3%. This outbreak was surprising: it happened immediately after the installation in a new hospital and the reinforcement of nosocomial infection surveillance (systematic screening of every patient admitted to the I.U.C., his isolation if he presents risk factors to multiresistant germs, increasing of handwashing stations). The overlapping period of hospitalisation concerning the 13 patients being reported as SARM carrier, having the same antibiogram, and the epidemic curve suggested a cross contamination. The index case was a MRSA carrier the day of her admission and have had a recent hospitalisation in a high risk unit. MRSA has always been isolated in nasal swab. Six patients among the thirteen carriers developed an infection and have been treated by vancomycin: two systemic infections and four pulmonary infections. The mortality rate was 33% and only one of them seemed to be directly due to MRSA. Area samples were all negative. The clinical staff have been screened with nasal swab. We identified only one nasal MRSA carrier. The pulsed-field gel electrophoresis study showed that 9/11 which have been analysed were identical. This outbreak brought about staff, more sensibilisation to the nosocomial infection and updating of plain hygien rules leaded to its stop five months later.

Hearing fluctuation during migraine attacks. Activity of propranolol-HCl in rats.

Transitory hearing impairment has been well documented in humans during basilar migraine attacks. Ischemia induced by activation of central nervous system adrenoreceptors by cAMP is one of the mechanisms that has been implicated, as well as calcium metabolism alterations. Propranolol-HCl has proven to be an effective treatment. Massive local adrenaline release is regarded as the primum movens mechanism triggering the liberation of other beta-receptor activators resulting in sterile edema and exudate. This exudate can be visualized (via ophthalmoscope) and is viewed as pathognomonic of a migraine attack. We investigated both the action of adrenaline and Propranolol-HCl on brainstem auditory potentials in 3 groups of young rats. The first group was perfused intra-arterially with adrenaline. The second group received the same treatment plus a prophylactic daily dose of Propranolol-HCl. The third group served as the control and received Propranolol-HCl, but was perfused with a Ringer solution. Alterations in blood flow and hearing sensitivity (BERA) following perfusion occurred in the first group only. Propranolol seems to exhibit a protective action during experimental attempts to induce migraine-like attacks in rats.

Three potassium currents in mouse motor nerve terminals.

A study of the K conductance of the presynaptic membrane has been performed in the triangularis sterni muscle of the mouse. External currents generated in the presynaptic terminals upon invasion by action potentials have been recorded using microelectrodes inserted into the perineurium of preterminal nerve bundles. The voltage-dependent K current could be pharmacologically dissected into fast (IKf) and slow (IKs) components. While both are sensitive to 3,4-diaminopyridine (3,4-DAP), only IKf is sensitive to tetraethylammonium (TEA). Uranyl (100-200 microM) and guanidine (5-10 mM) produced a near complete block of IKf and IKs, which can explain their facilitatory effect upon transmitter release. The third K current of presynaptic terminals is Ca2+-dependent, but was activated also by Sr2+. This current could be suppressed by nanomolar doses of charybdotoxin; it is also sensitive to TEA but not to 3,4-DAP, uranyl or guanidine.

Depression of calcium current at mouse motor nerve endings by polycationic antibiotics.

The hypothesis according to which polycationic antibiotics produce neuromuscular block by interfering with the Ca current of motor nerve terminals has been examined using external electrodes in nerve-muscle preparations of the mouse. It was found that kanamycin, bekanamycin and polymyxin B depressed presynaptic Ca currents probably by neutralizing negative surface charges.

Perilymphatic calcium and VIII nerve action potentials during gentamicin bolus i.v. injections. A preliminary study.

Life-threatening human sepsis is often treated using bolus intravenous aminoglycoside injections with transient deafness as a reported side effect. Young adult cats were given various high dosages of gentamicin in bolus injections (1 ml in 30 s). Scala vestibuli calcium and gentamicin, blood gentamicin and compound action potentials of the VIII nerve were measured shortly after the injections and 45 min later. An obvious relationship could be demonstrated between levels of gentamicin, decreased calcium content and acoustic thresholds elevation. Even after a high dose of 175 mg/kg that abolished action potentials at t = 2 min, recovery invariably occurred. It is believed that the reported transient hearing loss in humans may be partly attributable to a temporary blockage of calcium by gentamicin.