Neumonía bacterémica por Neisseria meningitidis: primer caso reportado en Chile y revisión bibliográfica / Neisseria meningitidis pneumonia. a case report

Few cases of bacteremic pneumonia by Neisseria meningitidis (NM) have been described worldwide; mostly in elderly patients or those with comorbidities. They appear clinically indistinguishable from other acute infectious pneumoniae, that do not develope the syndrome of meningococcemia. We report a 17-years-old male, without prior medical history, consulting in the emergency department with a 7-day history of productive cough, right pleural pain, fever and dyspnea. He was admitted to the ICU due to septic shock and respiratory distress. He was managed with vasoactive drugs and prone positioning ventilation for 48 hours. Chest radiography showed a right superior lobe condensation. The electrocardiogram and echocardiogram suggested septic myocarditis. Blood cultures demonstrated the presence of serogroup W135-NM. A lumbar puncture ruled out meningitis, and a 10-day ceftriaxone therapy was completed favorably.

Neuroprotección mediada por BDNF y óxido nítrico frente a excitotoxicidad en neuronas corticales e hipocampales / BDNF and nitric oxide-mediated neuroprotection against excitotoxicity in cortical and hippocampal neurons

En la epilepsia del lóbulo temporal (ELT), el hipocampo y estructuras temporales adyacentes se convierten en foco epiléptico, lo que ocurre después de un insulto cerebral, como una convulsión prolongada (o Status Epilepticus [SE]). Posterior al insulto, en el hipocampo ocurre muerte neuronal por excitotoxicidad, es decir, por sobre estimulación de receptores glutamatérgicos tipo NMDA (R-NMDA) y síntesis de óxido nítrico (NO) por la óxido nítrico sintasa neuronal (nNOS), una enzima dependiente de calcio. Sin embargo, otras estructuras cerebrales, como la corteza cerebral, son más resistentes al daño excitotóxico. Postulamos que esta menor susceptibilidad de la corteza cerebral a la excitotoxicidad, se debería a neuroprotección dependiente de la neurotrofina BDNF, que se sabe estimula la sobrevida neuronal. Se utilizaron cultivos neuronales primarios de hipocampo y corteza cerebral. Para evaluar excitotoxicidad, se agregó NMDA 30 uM. Se utilizaron estrategias farmacológicas para poner a prueba esta hipótesis, como el uso de L-NNA (inhibidor NOS), y TrkB-Fc (atrapador de BDNF). Se evaluó el porcentaje de sobrevida celular mediante el test de exclusión de Azul de Tripán. La viabilidad de los cultivos después de agregar NMDA fueron: corticales 71,2 +/- 2,8 por ciento, hipocampales 24,6 +/- 2,2 por ciento (p<0,01). Al inhibir la NOS, la viabilidad fue: corticales 31 +/- 6,5 por ciento, hipocampales 79,2 +/- 5,4 por ciento (p<0,01). En ausencia de BDNF fue: corticales 28,7+/- 7,9 por ciento, hipocampales 88,9 +/- 3 por ciento (p<0,01). Concluimos que después de un insulto excitotóxico, BDNF/NO son neuroprotectores en neuronas corticales pero no hipocampales. La potenciación de mecanismos neuroprotectores podría ser una alternativa terapéutica en patologías que involucran muerte neuronal por excitotoxicidad.

In temporal-lobe epilepsy (TLE), the hippocampus and adjacent temporal structures become an epileptic focus following a brain insult, such as a prolonged seizure (or Status Epilepticus). After the insult, neuronal death by excitotoxicity ocurrs, this is, by over stimulation of NMDA-type glutamate receptors (R-NMDA) and nitric oxide sinthesis by neuronal nitric oxide synthase (nNOS), a calcium-dependant enzyme. However, other brain structures, such as the cerebral cortex, are much more resistant to an excitotoxic challenge. We propose that the decreased susceptibility of the cerebral cortex could be explained by neuroprotection mediated by the neurotrophin BDNF, which is known to stimulate neuronal survival. Primary hippocampal and cortical neuronalcultures were used. To evaluate excitotoxicity, 30 uM NMDA was added. The signaling pathways to be tested were inhibited by using pharmacological inhibitors: L-NNA (NOS inhibitor), and TrkB-Fc, a BDN-scavenger. Percentages of cellular survival were evaluated using the Trypan Blue exclusion test. The viability of the cultures after adding NMDA was: larger in cortical than in hippocampal cultures, 71,2 +/- 2,8 percent for cortical and 24,6 +/- 2,2 percent hippocampal cells (p<0,01). When inhibiting NOS, the viability was: 31 +/- 6,5 percent for cortical and 79,2 +/- 5,4 percent for hippocampal cells (p<0,01). In absence of BDNF, 28,7 +/- 7,9 percent of the cortical cells survived, while in the hippocampal cultures it was of 88,9 +/- 3 percent (p<0,01). We conclude that after an excitotoxic insult, BDNF/NO are neuroprotective in cortical but not hippocampal neurons. The potentiation of such neuroprotective mecanisms could be used as a therapeutic alternative in pathologies that involve neuronal death by excitotoxicity.