W. Lew

Significance of Salmonella in Ulcerative Cecitis of Rats.

Summary It appears, then, that no proof has been brought that salmonella is the cause of ulcerative cecitis of rats. In our laboratory a specific strain of salmonella was, to be sure, intimately associated with the lesions and this organism further was shown to be pathogenic for rats, since an acute diffuse enteritis was readily produced and the organism was again recovered from the lesions. Chronic cecitis, however, failed to develop to a significantly greater extent than in untreated controls. It is possible that some other agent is the primary cause of cecitis and that salmonella is merely an associated organism or one which tends to act as a secondary invader. Further search for such a primary agent is in progress.

Relation of a Specific Strain of Salmonella to Ulcerative Cecitis of Rats

Summary 1. A specific strain of salmonella has been invariably obtained on culture from the ulcers of rat cecitis, 2. Salmonella were not obtained from the cecum in the absence of lesions with one exception. 3. Agglutinins for the specific strain of salmonella are found in most of the rats in this colony although the titer is on the average higher in animals with visible cecitis. 4. Feeding the specific salmonella in appropriate doses was followed after a long latent period by development of cecitis in many of the test animals. 5. The association of some other synergistic agent is not fully excluded but seems at present unlikely.

Prophylactic Effect of Sulfaguanidine Against Ulcerative Cecitis in Rats

Discussion and Summary Chronic ulcerative cecitis, as it developed spontaneously in a rat colony, presented itself as an ideal experimental disease in which to study the effect of chemotherapy. At the time of the present observations the majority of the animals in our colony developed lesions of “cecitis” by the time they had reached 300+ g in weight. The addition of 0.5% of sulfaguanidine to the diet produced no deleterious clinical effect nor any visible gross lesions. On the contrary rats on sulfaguanidine gained weight rapidly. The drug even in the small doses used had a striking prophylactic effect against the development of cecitis; not only was the incidence very much lower than in the control group but, even more impressive, such lesions as occurred were minimal in contrast to the advanced disease found in most of the untreated rats. The protective effect of sulfaguanidine is demonstrated further by the failure of the treated animals to lose weight as did the controls with progressive lesions. The concentration of the drug in the stools was not measured but the relatively low blood levels suggest, as pointed out by Marshall 4 that sulfaguanidine is less readily absorbed than some of the other sulfonamides. In clinical work on ulcerative colitis, dysentery and other bowel infections in man we have not always been impressed with the therapeutic effects of sulfaguanidine. It is possible, however, that the drug may be of greater value as a prophylactic, and the present experiments suggest that such is the case. Trials in man under proper conditions would seem worth while in connection with military establishments.

Age and the Rate of Venous Enlargement under Increased Venous Pressure.

Conclusions 1. After ligation of the vena cava above the entrance of the renal veins a plot of the logarithms of the percentage mortality on age seems to indicate that they are a linear function of the age at the time of operation. 2. It is suggested that the above relation may be the result of a decrease in the rate of venous enlargement under increased pressure as age advances.

Prevention by Succinyl Sulfathiazole of Ulcerative Cecitis in Rats

Conclusion Succinyl sulfathiazole incorporated in the stock ration completely prevented the development of ulcerative cecitis in rats.