Influence of periplasmic oxidation of glucose on pyoverdine synthesis in Pseudomonas putida S11.

Fluorescent pseudomonads catabolize glucose simultaneously by two different pathways, namely, the oxidative pathway in periplasm and the phosphorylative pathway in cytoplasm. This study provides evidence for the role of glucose metabolism in the regulation of pyoverdine synthesis in Pseudomonas putida S11. We have characterized the influence of direct oxidation of glucose in periplasm on pyoverdine synthesis in P. putida S11. We identified a Tn5 transposon mutant of P. putida S11 showing increased pyoverdine production in minimal glucose medium (MGM). This mutant designated as IST1 had Tn5 insertion in glucose dehydrogenase (gcd) gene. To verify the role of periplasmic oxidation of glucose on pyoverdine synthesis, we constructed mutants S11 Gcd(-) and S11 PqqF(-) by antibiotic cassette mutagenesis. These mutants of P. putida S11 with loss of glucose dehydrogenase gene (gcd) or cofactor pyrroloquinoline quinone biosynthesis gene (pqqF) showed increased pyoverdine synthesis and impaired acid production in MGM. In minimal gluconate medium, the pyoverdine production of wild-type strain S11 and mutants S11 Gcd(-) and S11 PqqF(-) was higher than in MGM indicating that gluconate did not affect pyoverdine synthesis. In MGM containing PIPES-NaOH (pH 7.5) buffer which prevent pH changes due to gluconic acid production, strain S11 produced higher amount of pyoverdine similar to mutants S11 Gcd(-) and S11 PqqF(-). Therefore, it is proposed that periplasmic oxidation of glucose to gluconic acid decreases the pH of MGM and thereby influences pyoverdine synthesis of strain S11. The increased pyoverdine synthesis enhanced biotic and abiotic surface colonization of the strain S11.

Glucose 6-phosphate dehydrogenase deficiency with kernicterus: progressive late recovery from profound deafness.

In this case report a near-term infant with Glucose 6-Phosphate Dehydrogenase (G6-PD) deficiency had an unconjugated bilirubin level of 703 on the 11th day of life but maintained his haemoglobin levels above 11 gm/dl. At 4 months of age he demonstrated the clinical picture of Kernicterus: profound sensorineural deafness and evidence of encephalopathy. However, by 15 months of age his abnormal cerebral and motor signs had regressed to a near-normal level in parallel with a gradual improvement in hearing, which also reached normal levels, first in the right ear, then in the left. At this age residual mental retardation has not been excluded but his communication skills, though delayed by 4-6 months, were moving towards the level when they would be appropriate for his age.

Primaquina y viajeros del mundo arabe. Reporte y recomendación / Primaquine and travellers of the Arab world. Report and recommendations

Se reportan dos reacciones graves hemolíticas en 2 pacientes de origen árabe por el uso de la primaquina como parte del tratamiento presuntivo antipalúdico dado en Cuba a todos los viajeros procedentes de países con áreas endémicas de paludismo. Teniendo en cuenta la no existencia de casos importados de paludismo en viajeros procedentes del mundo árabe desde hace más de 15 años y en atención a la frecuencia de individuos deficientes de la enzima glucosa 6 fosfato deshidrogenasa, se recomienda la suspensión de este proceder presuntivo, con el mantenimiento del resto de las medidas de vigilancia, en los viajeros provenientes de dicha región (AU)

Estudio bioquímico y molecular de la glucosa-6-fosfato deshidrogenasa en Cuba / Biochemical and molecular study of glocose-6-phospate dehydrogenase in Cuba

Se realizó un estudio bioquímico y molecular de 17 pacientes del sexo masculino diagnosticados como deficientes de glucosa-6-fosfato deshidrogenasa (G6PD): 13 con la variante G6PD A- y 4 con variantes raras con movilidad electroforética rápida (caso 1, G6PD Caujerí; caso 2, G6PD Guantánamo). Se realizaron además otras pruebas de laboratorio. Basado en el porcentaje de la actividad enzimática y en el cuadro clínico, los 17 pacientes se agruparon en la clase 3. El estudio molecular de 13 pacientes con G6PD A-, de la G6PD Caujuerí y uno de los pacientes con posible variante rara, demostró las mutaciones en la nt 202. La G6PD Guantánamo y el otro paciente con variante electroforética rápida presentaron la segunda mutación en el nt 968. La detección de la G6PD A- en individuos de la raza blanca en distintos países puede ser debido a la llegada de un ancestro de origen africano hace cientos de años. El empleo del PCR es una técnica rápida, confiable y muy útil para el estudio de variantes polimórficas de G6PD (AU)

Acute renal failure amongst children in a tropical environment.

The pathogenetic factors leading to acute renal failure (ARF) in 223 children between the ages of 20 days and 14 years were studied. Diarrhoeal diseases were responsible for ARF in 49.8%, acute glomerulonephritis in 34.1%, drug induced intravascular hemolysis in glucose -6-phosphate dehydrogenase deficiency in 4.5%, snake bite in 4%, hemolytic uremic syndrome in 2.2%, and miscellaneous causes in 5.4%. Dialysis was instituted in 178 children and the others were treated conservatively. Renal histology in 39 out of 76 children who presented with an acute nephritic illness revealed acute endocapillary proliferative glomerulonephritis in 27 and crescentic glomerulonephritis in 12. The histology in 79 out of 147 remaining patients showed acute tubular necrosis in 64, acute cortical necrosis in 13, and acute interstitial nephritis in 2. Overall mortality was 27.4%. This high incidence of ARF due to infective diarrhoeas and dysentery reflects poor socio-economic and hygienic conditions, inadequate facilities in rural areas, delays in seeking medical advice, and lack of knowledge about fluid and electrolyte therapy amongst the staff.

Glucose-6-phosphate dehydrogenase revisited.

Hemolytic diseases associated with drugs have been recognized since antiquity. Many of these anemias have been associated with oxidizing agents and deficiencies in the intraerythrocytic enzyme glucose-6-phosphate dehydrogenase. This paper outlines the discovery, prevalence, and variants of this enzyme. Methods of diagnosis of associated anemias are offered.