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1.
Rev Neurol (Paris) ; 168(3): 239-56, 2012 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-22386676

RESUMEN

Malaria is still the world's major important parasitic disease and is responsible for the death of more people than any other communicable disease except tuberculosis. A major change in recent years has been the recognition that severe malaria, predominantly caused by Plasmodium falciparum, is a complex multi-system disorder presenting with a range of clinical features. Some surviving patients have an increased risk of neurological and cognitive deficits, behavioural difficulties and epilepsy, making cerebral malaria a leading cause of childhood neurodisability in the malaria transmission area. It is unclear how an intravascular parasite causes such brain injury. Understanding of these mechanisms is important to develop appropriate neuroprotective interventions. However, due to the high specificity of P. falciparum to the human host and to the fact that clinical studies in human are not always feasible, our knowledge about this syndrome mainly comes from autopsy studies which can only give us a limited view of this deadly syndrome. Efforts developed by the scientific community have shown that development of severe malaria probably results from a combination of parasite-specific factors such as adhesion and sequestration to the vascular endothelium, the release of bioactive molecules, together with host inflammatory responses and metabolic acidosis. Recent studies have shown that endothelial cells could play a central role in the onset of the severe malaria. Indeed, adhesion of parasitized erythrocytes to these cells could drive their activation, which could participate in the trigger of an immune response and haemostatic derangements. Moreover, death of endothelial cells could be at the origin of the blood-lung/brain barrier breakdown. Despite the efforts to find new mechanisms, which explain the physiopathology of severe malaria, research progress is slowed down by the lack of experimental models, which reproduce this complex multi-system disorder. In absence of a vaccine so far, the rapid diagnosis of the disease, an efficient treatment, a correct management and nursing care are the only weapons to control mortality due to P. falciparum. It is important to note that in the future, the treatment of severe malaria may involve adjuvant treatments in addition to a potent antimalarial drug. In the present review, we summarize both what is known and practically useful for a physician, and the most promising and current topics of research.


Asunto(s)
Malaria Cerebral/terapia , Adulto , Animales , Antimaláricos/uso terapéutico , Niño , Costo de Enfermedad , Modelos Animales de Enfermedad , Femenino , Haplorrinos , Humanos , Control de Infecciones , Malaria Cerebral/complicaciones , Malaria Cerebral/diagnóstico , Malaria Cerebral/epidemiología , Malaria Cerebral/parasitología , Ratones , Plasmodium falciparum/fisiología , Embarazo , Pronóstico
2.
New Microbes New Infect ; 38: 100796, 2020 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-33294192

RESUMEN

We describe a new strain named Bartonella gabonensis sp. nov. strain 669T (CSURB1083). The entire genome of this strain is described here. It was isolated from a savannah rodent, a brush-furred rat (Lophuromys sp.), trapped the city of Franceville in Gabon, in Central Africa. B. gabonensis is an aerobic, rod-shaped and Gram-negative bacterium. On the basis of the organism's features, and following a taxonogenomic approach, we propose the creation of the species Bartonella gabonensis sp. nov.

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