Involvement of the Upper Respiratory Tract in Orally Induced Salmonellosis in Mice

examined. Viable counts of Salmonella in the local lymphoid tissues and draining nodes indicated that the ileal Peyer's patches were primarily involved in the development of a subsequent enteric fever, irrespective of the method of oral challenge. Contamination of drinking water with a high concentration of salmonellae produced infection of the ileal Peyer's patches and the eventual development of systemic disease. The cervical lymph nodes were sporadically involved early in the infection, but this involvement soon became general, with large numbers of salmonellae in the cervical nodes by 36 hr. A lower concentration of salmonellae in drinking water led to primary involvement of the ileal Peyer's patches; upper respiratory tract involvement was detected much later in the infection. Intragastrically infected mice exhibited the same low-level infection of the cervical lymph nodes as that in mice infected via drinking water. Thus systemic infection apparently results from infection of the ileal Peyer's patches; a small percentage of the animals develop a concurrent upper respiratory tract infection that may be responsible for the development of carrier states after enteric infections. A satisfactory animal model of any infectious disease of humans should always mirror the natural infection as closely as possible. In studies of immunity to human typhoid fever, a mouse model has frequently been used, but several important differences from the naturally acquired disease render many of the laboratory findings less meaningful [1]. Studies in this laboratory have obviated many of the objections raised by the use of such procedures [2]. Nevertheless, it may be fairly said that an intragastrically administered inoculum may represent an artificial model of enteric fever, since the human disease is not contracted in this way. By deposition of the infectious dose direcly into the stomach by means of a feeding needle, the possible entry of organisms into the host by alternative routes is avoided; thus events in the development of systemic infection may be improperly understood simply because attention is focused away from nonintestinal entry sites. After intragastric administration of virulent salmonellae, the challenge organisms enter the system by way of the ileal Peyer's patches and their draining lymph nodes [3]. Thus the initial site of bacterial multiplication involves only the lymphoid accumulations within a circumscribed area of the terminal small intestine; areas more anterior to this section do not appear to be affected, at least in the early stages of infection. However, when the salmonella culture is ingested naturally, there is a strong possibility of involvement of lymphoid aggregations associated with the esophagus and/or the respira