Distal tibial physeal arrest after meningococcal septicaemia: management and outcome in seven ankles.

Survivors of infantile meningococcal septicaemia often develop progressive skeletal deformity as a result of physeal damage at many sites, particularly in the lower limb. Distal tibial physeal arrest typically occurs with sparing of the distal fibular physis leading to a rapidly progressive varus deformity. There have been reports of isolated cases of this deformity, but to our knowledge there have been no papers which specifically describe the development of the deformity and the options for treatment. Surgery to correct this deformity is complex because of the patient's age, previous scarring and the multiplanar nature of the deformity. The surgical goal is to restore leg-length equality and the mechanical axis at the end of growth. Surgery should be planned and staged throughout growth in order to achieve the best functional results. We report our experience in six patients (seven ankles) with this deformity, who were managed by corrective osteotomy using a programmable circular fixator.

Susceptibility of captive adult winter-run Chinook salmon Oncorhynchus tshawytscha to waterborne exposures with infectious hematopoietic necrosis virus (IHNV).

Sexually mature female Chinook salmon Oncorhynchus tshawytscha with no prior history of exposure to infectious hematopoietic necrosis virus (IHNV) were susceptible to experimental infection induced by additions of virus to the water. The resulting infections resembled those observed among naturally infected hatchery and wild populations of Chinook salmon. Virus was detected as early as 4 d post-exposure (p.e.) and subsequently in all virus-exposed fish that died or that were examined at 14 d p.e. when the study was terminated. The greatest concentrations of virus, up to 10(8) plaque-forming units (pfu) ml(-1), were found in the ovarian fluid at 13 to 14 d p.e., but the virus was also found in high concentrations in the gill, kidney/spleen and plasma. In contrast, the virus was not recovered from unexposed control adult salmon that died or were sampled at the end of the study. Despite detecting concentrations of IHNV in excess of 10(7) pfu g(-1) of tissue, no specific microscopic lesions were found in IHNV-exposed compared to unexposed control salmon. The results of this initial study suggest that virus in the spawning environment, either from adult salmon or other sources, may contribute to its rapid spread among adult Chinook salmon, thereby considerably increasing the prevalence of IHNV infection in both wild and hatchery populations of adult Chinook salmon.