444 Pathogenesis o£ Undiilant Fever 



the suspicion of cholecystitis, it infrequently remains undecided as to whether 

 the icterus is caused by increased bilirubin formation or insufficiency of the 

 liver cells. Schlierbach and Wurm'^ mention a Bang infection which appeared 

 with the symptoms of a "catarrhal jaundice." 



Both the direct and indirect van den Bergh reactions were positive in 

 the blood plasma of D.S. An excess of urobilinogen in the urine would suggest 

 that the jaundice resulted from overproduction of bile pigment. As essential 

 factors, one might suspect the fever associated with anoxemia which depresses 

 the function of the hepatic cells. On the other hand, the direct-reacting plasma- 

 bilirubin was demonstrable in the blood. Thus the widespread necrosis of 

 liver cells was followed by leakage of bilirubin from the canaliculi into the 

 blood. Overproduction led to retention and later to hepatic damage with 

 subsequent regurgitation. 



In the future the faintly marked jaundice— which may be observed in the 

 course of a Brucella infection— should be carefully analyzed in order that the 

 etiology and pathogenesis may be clarified. It is becoming increasingly evi- 

 dent that the term "catarrhal jaundice" has been applied to a mixture of 

 different etiologies. From the facts thus far available, it is clear that a moderate 

 retention jaundice due to overproduction of bilirubin is a common symptom 

 of brucellosis. 



The bile contained in the gall bladder at autopsy yielded 30,000 Brucella 

 organisms per cubic centimeter. It is not unlikely that, just as may be the case in 

 typhoid fever, this viscus becomes the seat of prolonged harborage and prolifer- 

 ation of the Brucella organisms (Kennedy," Eyre," and others). In fact, in quite 

 a few instances it has bcome necessary to remove the gall bladder to relieve the 

 patient and to accelerate recovery (Bull and Gram;" Simpson;^* Hardy and 

 associates;" Leavell and Amoss;" Amoss;" Mettier and Kerr;'" Menefee and 

 Boston;"" and others). Unpublished experiments on rabbits and on guinea pigs 

 indicate that intravenously inoculated Brucella organisms promptly appear 

 in the bile. The larger the inoculum the greater the shedding of bacteria in 

 the bile of the common duct or the acciunulations in the cystic bile. Thus the 

 hemato-hepatic route is the usual one in the animal and in all probability 

 also in man. From what is known concerning the pathogenesis of cholecystitis, 

 it would indeed have been a miracle if this organ had escaped invasion in the 

 presence of a blood-stream infection of over 1,700 organisms per cubic centi- 

 meter. A careful search for embolic-metastatic foci throughout the mucosa of 

 the gall bladder was entirely negative. However, it should be remembered that 

 with the progress of the inflammatory reactions in the liver, the biliary ap- 

 pendices may become involved. The persistence of the Brucella bile-carrier 

 state in all probability depends on the degree of the inflammation of the gall- 

 bladder wall. 



It was noted that the portal lymph nodes were definitely enlarged and 

 hyperemic. Significant lesions in the form of a desquamative process in the 

 cortical sinuses and the early aggregations of mononuclear cells and a few 



