[Vaccinations in sports and recommendations for immunization against flu, hepatitis A and hepatitis B].

Intensive physical training in elite athletes can have an adverse effect on the immune system, and can increase the susceptibility to infectious diseases. The insult to the immune system includes the cellular, humoral and phagocitic pathways. The increased incidence of viral infections (in particularly of the upper respiratory tract) occurs mainly during periods of intense exercise training and competitions due to the combination of physiological and psychological stress. Other factors that may contribute to the decreased immunity and increased susceptibility to infections include eating disorders and nutritional deficiencies, jet lag, sleep deprivation, and lack of proper hygiene in shared food and sleeping quarters. For elite athletes, even a mild viral infection can be devastating due to loss of important training hours and/or compromise of competitive performance. Therefore, in addition to the goal of improving the athletes performance, another important responsibility/obligation of the staff working with athletes (physicians, nutritionists, physiotherapists, and psychologists), is to emphasize preventive medicine and maintenance of good health. In this article we define athletes, and especially elite athletes, as a population at risk of various infections, and recommend immunization against hepatitis A and B and a yearly immunization against influenza.

A new exon 9 glucose-6-phosphate dehydrogenase mutation (G6PD "Rehovot") in a Jewish Ethiopian family with variable phenotypes.

Hereditary nonspherocytic hemolytic anemia (HNSHA) is a rare manifestation of glucose-6-phosphate dehydrogenase (G6PD) gene mutations, caused mainly by mutations located in exon 10 of the G6PD gene and less commonly by mutations in other parts of the gene. A new, exon 9, single-base mutation representing a T --> C transition at cDNA nucleotide 964 was found in three brothers and their carrier mother of Jewish Ethiopian descent. Biochemical characterization of the resultant protein was not performed. Though clinical manifestations included HNSHA in all cases, the severity of hemolysis and the transfusion requirement differed markedly. Severe congenital neutropenia (Kostmann's syndrome)--a disorder never reported before in conjunction with G6PD deficiency--was observed in one case. Levels of white blood cell G6PD activity of the three patients were 0-5% of normal controls. Neutrophil oxidative and bactericidal activities were inherently impaired in the patient with Kostmann's syndrome, but were well preserved in his two siblings.