4 research outputs found

    The essential peptidoglycan glycosyltransferase MurG forms a complex with proteins involved in lateral envelope growth as well as with proteins involved in cell division in Escherichia coli

    Get PDF
    In Escherichia coli many enzymes including MurG are directly involved in the synthesis and assembly of peptidoglycan. MurG is an essential glycosyltransferase catalysing the last intracellular step of peptidoglycan synthesis. To elucidate its role during elongation and division events, localization of MurG using immunofluorescence microscopy was performed. MurG exhibited a random distribution in the cell envelope with a relatively higher intensity at the division site. This mid-cell localization was dependent on the presence of a mature divisome. Its localization in the lateral cell wall appeared to require the presence of MreCD. This could be indicative of a potential interaction between MurG and other proteins. Investigating this by immunoprecipitation revealed the association of MurG with MreB and MraY in the same protein complex. In view of this, the loss of rod shape of ΔmreBCD strain could be ascribed to the loss of MurG membrane localization. Consequently, this could prevent the localized supply of the lipid II precursor to the peptidoglycan synthesizing machinery involved in cell elongation. It is postulated that the involvement of MurG in the peptidoglycan synthesis concurs with two complexes, one implicated in cell elongation and the other in division. A model representing the first complex is proposed

    Intoxicação em suínos pela ingestão de sementes de Aeschynomene indica (Leg.Papilionoideae) Poisoning in swine from the ingestion of Aeschynomene indica (Leg.Papilionoideae) seeds

    No full text
    Relata-se um surto espontĂąneo de intoxicação em suĂ­nos pela ingestĂŁo de sementes de Aeschynomene indica e a reprodução da doença nessa espĂ©cie animal. O surto espontĂąneo ocorreu numa propriedade de criação de suĂ­nos localizada na regiĂŁo central do Rio Grande do Sul. Nessa propriedade havia 100 suĂ­nos (20 matrizes e 80 suĂ­nos jovens de vĂĄrias categorias). Os suĂ­nos eram alimentados com uma ração feita na propriedade pela mistura de 50% farelo de milho, 25% de farelo de soja, 5% de um suplemento vitamĂ­nico-mineral de origem comercial e 20% quirera de arroz contaminada por 40% de sementes de A. indica. Embora aparentemente todos os suĂ­nos tenham recebido a mesma ração, apenas os suĂ­nos de 45 dias de idade foram afetados; as taxas de morbidade, mortalidade e letalidade foram respectivamente 25%-40%, 8,5%-20% e 25%-66%. Os sinais clĂ­nicos apareceram cerca de 24 horas apĂłs o inĂ­cio da administração da ração contendo sementes de A. indica e incluĂ­am vĂĄrios graus de incoordenação no andar, quedas, decĂșbito esternal com membros pĂ©lvicos posicionados afastados entre si, decĂșbito lateral e morte. NĂŁo foi possĂ­vel determinar quantos suĂ­nos se recuperaram e quanto tempo levou a recuperação. Um suĂ­no foi submetido Ă  eutanĂĄsia e necropsiado na propriedade. A doença foi reproduzida em 5 suĂ­nos jovens (A-E) alimentados com uma ração contendo 10% (SuĂ­no A), 15% (SuĂ­no B) e 20% (SuĂ­nos C-E) de sementes de A. indica e em um suĂ­no mais velho (SuĂ­no F) que recebeu uma ração com 16,5% de sementes de A. indica. Os sinais clĂ­nicos foram semelhantes aos observados nos suĂ­nos do surto espontĂąneo. Os SuĂ­nos A, B e F foram submetidos Ă  eutanĂĄsia e os SuĂ­nos C-E morreram de uma doença aguda respectivamente 16, 21 e 24 horas apĂłs o inĂ­cio do experimento. Os achados de necropsia incluĂ­am acentuada hiperemia das leptomeninges em todos os suĂ­nos, grandes quantidades de sementes de A. indica no estĂŽmago e avermelhamento transmural da parede do intestino e conteĂșdo intestinal sanguinolento nos SuĂ­nos C-E. Um hematoma foi observado no pulmĂŁo do SuĂ­no C. Os achados histopatolĂłgicos no encĂ©falo dos suĂ­nos alimentados com as maiores concentraçÔes (20%) de sementes de A. indica (C-E) consistiram em ĂĄreas focais e simĂ©tricas de congestĂŁo, edema, hemorragia e tumefação do endotĂ©lio vascular em diversos nĂșcleos e no cĂłrtex telencefĂĄlico. Nos SuĂ­nos A e B, que receberam menores concentraçÔes das sementes de A. indica, e no SuĂ­no F, caso espontĂąneo da doença, as alteraçÔes histolĂłgicas no encĂ©falo consistiam de ĂĄreas bem definidas de malacia focal simĂ©trica; nessas ĂĄreas a neurĂłpila normal era obliterada por numerosos macrĂłfagos espumosos dispostos em estreita aposição, astrocitose e capilares com endotĂ©lios tumefeitos. Os focos de malacia focal simĂ©trica em suĂ­nos intoxicados com sementes de A. indica afetavam os nĂșcleos cerebelares e vestibulares, a substĂąncia negra, o putĂąmen e os nĂșcleos mesencefĂĄlicos, oculomotor e nĂșcleo vermelho. Esses dados indicam que a ingestĂŁo de sementes de A. indica Ă© responsĂĄvel por essa condição neurolĂłgica, que a doença pode ser fatal e que parece afetar igualmente suĂ­nos jovens e adultos. O desenlace clĂ­nico e as alteraçÔes patolĂłgicas sĂŁo dependentes da dose e as lesĂ”es encefĂĄlicas progridem de danos vasculares a edema vasogĂȘnico, hemorragia e malacia.<br>A spontaneous outbreak of a neurological disease in swine caused by the ingestion of Aeschynomene indica seeds and the reproduction of the disease in the same animal species are reported. The natural outbreak occurred in a pig-raising facility in the central region of the state of Rio Grande do Sul, Brazil. On the premises there were 100 pigs (20 breeding sows and 80 young weaned pigs from several categories) that were fed a ration made by mixing 50% of corn bran, 25% of soybean bran, 5% of a commercial mix of vitamins and minerals, and 20% of broken rice contaminated with 40% of A. indica seeds. Although all pigs apparently ingested the same ration, only 45-day-old pigs were affected; morbidity, mortality and lethality rates were respectively 25%-40%, 8.5%-20%; and 25%-66%. Clinical signs appeared 24 hours after the beginning of feeding of A. indica seeds contaminated ration and included variable degrees of incoordinated gait, falls, sternal recumbency with the hind limbs in a wide base stance, lateral recumbency and death. It was not possible to ascertain how many pigs recovered nor the time frame of recovery. One pig was euthanatized and necropsied in the premises. The poisoning was reproduced in 5 young pigs (A-E) which were fed a ration containing 10% (Pig A), 15% (Pig B) and 20% (Pigs C-E) of A. indica seeds, and in one older pig (Pig F) which was fed a ration with 16.5% of A. indica seeds. Pigs A, B and F were euthanatized and Pigs C-E died of an acute disease respectively 16, 21 and 24 hours after the beginning of the experiment. Clinical signs were similar to those observed in pigs of the spontaneous outbreak. Necropsy findings included marked hyperemia of the encephalic leptomeninges of all pigs; there were large amounts of A. indica seeds in the stomach and reddening of the intestinal wall and bloody intestinal content in Pigs C-E. A hematoma was observed in the lungs of Pig C. The histopathological findings in the brain of pigs fed rations with larger concentrations (20%) of A. indica seeds (C-E) included congestion, edema and hemorrhage and swollen vascular endothelia with focal symmetrical distribution in several brain nuclei and in the telencephalic cortex. In Pigs A and B, and in Pig F, the case which received the lower dosage of the seeds of A. indica, and in the pig from the spontaneous outbreak, histopathological changes in the brain consisted of discrete focal symmetrical areas of malacia in which closely packed Gitter cells and astrocytosis, and capillaries with swollen endothelium obliterated the normal neuropil. The symmetrical malacic foci caused by the ingestion of A. indica seeds in swine affected cerebellar and vestibular nuclei, putamen, and the mesencephalic oculomotor and red nuclei. This indicates that the A. indica seeds ingestion was responsible for the neurological condition, that it may be fatal and seems to affect equally young and older swine. The clinical outcome and pathological changes were dose-dependent, and the brain lesions progressed from damaged blood vessels to vasogenic edema, hemorrhage and malacia
    corecore