Lethal challenge of gnotobiotic weanling rats.

Lethal challenge of gnotobiotic weanling rats I am surprised that a more critical appraisal of the paper by Lee et al' was not made prior to publication. The paper is poorly constructed and the conclusions invalid. The mixing of the commensal organisms obtained from the nasopharynx of different infants who had died as a result of SIDS, and injecting them subcutaneously in high concentrations (lO9/l) and high dose (0-2 ml) cannot be used to explain the phenomenon of sudden unexpected death in infancy. The authors state that their histology results showed typical inflammatory features in lungs, liver, and heart muscle: such findings are never seen in SIDS. The authors state in their discussion that: "we found minimal histological evidence of respiratory inflammation ............. a situation analogous to SIDS." Once again, such inflammatory changes are not a feature in cases of SIDS. The authors state that: "bacteria were, however, recovered after death, indicating that the animals had died with septicaemia." Cases of SIDS never die as a result of septicaemia. I therefore cannot agree with their conclusion that: "the sudden death ofthe animal is similar clinically and histologically to SIDS in human infants." Inducing a sep-ticaemia death in a germ free weanling rat bears very little relation to sudden unexpected deaths in infancy. Telford DR. Lethal challenge of gnotobiotic weanling rats with bacterial isolates from cases ofsudden infant death syndrome. The aim of our investigation was to produce an animal model of sudden infant death syndrome (SIDS) by exposing gnotobiotic weanling rats to bacterial isolates from cases of SIDS cases. The criteria of a successful model, decided in advance were: (i) rapid death; (ii) minimal histological changes at necropsy; and (iii) no recovery of viable bacteria after death. Our results show modest success with the first two criteria but not the third. The extent to which the findings deviate from the ideal are clearly stated in the paper, and Dr Wayte's criticisms , in so far as they are accurate and pertinent, merely restate the points we emphasised. His statements on the histological changes are, however, far from accurate. In SIDS it is not uncommon to find a few inflammatory cells in the liver sinusoids, portal tracts, and bladder submucosa, occasional lymphocytes in cardiac muscle, and rather more pronounced inflammation in the upper and lower respiratory tracts.'3 These findings have been described by many authors. The histo-logical changes in the rats, …