STUDIES ON UROBILIN PHYSIOLOGY AND PATHOLOGY

A variety of evidence is presented, all of which supports the view that in the uninfected animal the intestinal tract is the only place of origin of urobilin, not merely under normal circumstances, but when there is biliary obstruction. Animals rendered urobilin-free by collection of all of the bile from the intubated common duct remain urobilin-free even after severe hepatic injury. In our experiments urobilinuria was never found after liver damage except when bile pigment was present in the intestine. Thus, for example, it appeared during the first days after Ugation of the common duct, but disappeared as the stools became acholic. When this had happened a small amount of urobilin-free bile, given by mouth, precipitated a prompt urobilinuria. After obstruction of the duct from one-third of the liver, mild urobilinuria was found, but no bilirubinuria. In animals intubated for the collection of a part of the bile only, while the rest flowed to the duodenum through the ordinary channels, liver injury caused urobilinuria, unless indeed it was so severe as to lead to bile suppression, when almost at once the urobilinuria ceased, though the organism became jaundiced. The evidence here presented, when taken with that of our previous papers, clearly proves that urobilinuria is an expression of the inability of the liver cells to remove from circulation the urobilin brought by the portal stream, with result that the pigment passes on to kidney and urine. Urobilinuria occurs with a far less degree of liver injury than does bilirubinuria. Our work has, for the most part, been carried out with animals having uninfected livers and bile passages. But the influence of cholangitis with infection has been briefly discussed in the light of some preliminary observations. The influence of infection on the place of formation of urobilin and on the occurrence of urobilinuria will form the subject of another communication.

Notes onTrypanosoma lewisiand its Relation to CertainArthropoda

1.Trypanosoma lewisiwas found in 25% of rats caught in and about Cambridge. Of these rats 12% were young, 33% adult, and 29% old. In this region the endetnicity was localised to certain areas.2. Fleas (C. fasciatusandC. agyrtes) were constantly found associated with wild rats infected withT. lewisi. We think that these two species of fleas are the chief carriers of the parasite from rat to rat in this region.3. We tried transmission experiments with fleas (C. fasciatusandC. agyrtes), lice (H. spinulosus), bugs (A. lectularia), ticks (O. moubata, nymphs and adults), andGamasussp., but only obtained a positive result by the agency of fleas.4. In the transmission experiments the arthropod was transferred from an infected to an uninfected animal. 16% of 138 experiments with fleas were successful, 80—98% of the fleas used were non-infective, while 2—20% were infective.5. Distant transmission occurs with fleas. This was observed by one of us in January, 1909.6. ‘Mechanical’ transmission occurs sometimes with fleas.7. Infective fleas do not transmit the power of infection to their young.8. The mechanism of infection in the case of mechanical transmission is by the bite of the flea; in the case of the distant infection it is not so.9. The infective forms ofT. lewisifor distant transmission are probably the ‘small trypanosomes’ which we have described elsewhere (1910). The forms ofT. lewisifound prior to the small trypanosomes in the developmental cycle are not infective.10. The development of the trypanosomes in the flea is not interfered with by the flea feeding on a rat immune to the disease.11. Seventeen experiments with lice were performed, but no transmission was obtained by their agency. 1139 lice were used. No confirmation of Baldrey's infective cycle in lice could be obtained.12. We could trace no connection between transmission of infection by lice and the presence in them of ‘developmental forms.’13. No transmission ofT. lewisiby other arthropods was obtained. These negative results had no connection with the presence in the arthropods of ‘developmental forms.’In conclusion we would like to thank Professor Nuttall for his kindness in inoculating our animals and providing us with the material for our experiments, and for his interest and advice in our work.