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We recently demonstrated that the cysteine proteinase inhibitor, E-64, sensitizes human Burkitt's lymphoma (Daudi) to the antitumor action of bleomycin (BLM) by blocking its metabolism. We now report that E-64 sensitizes the BLM resistant human lung carcinoma A-549 by a mechanism unrelated to the inhibition of BLM metabolism. Treatment of A-549 tumor-bearing nude mice with either BLM (10 mg/kg) or E-64 (40 mg/kg) every other day for 10 days did not inhibit tumor growth. However, a 30 min pretreatment with E-64 prior to BLM caused complete and sustained inhibition of tumor growth. In contrast to our results with Burkitt's lymphoma, E-64 did not inhibit BLM metabolism but rather enhanced the tumor accumulation of BLM; within 10 min of BLM administration, tumors from E-64 pretreated mice showed a 6-fold higher accumulation of BLM A2 compared to non-pretreated xenografts. Furthermore, the level of tumor-associated BLM A2 remained 2-fold higher in E-64 pretreated mice 20 and 30 min after BLM administration. In E-64 pretreated mice, the plasma level of BLM was increased by 2-fold. These results demonstrate that the cysteine proteinase inhibitor, E-64, sensitized human lung carcinoma A-549 to BLM and, contrary to the expected mechanism, this effect of E-64 was not related to the inhibition of BLM metabolism.

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No new serotypes have been added to the Shigella schema since 1958, although several provisional serotypes have been described. We conducted biochemical and serological studies on three provisional Shigella boydii serotypes. Four strains of serotype 2710-54 from four widely separated countries, 7 strains of serotype 3615-53 from three different countries, and 31 strains of serotype 1344-78 (E10163) from six different countries were included. Reactions of all three serotypes were consistent with those of S. boydii. On the basis of these results and other published research, we propose that these three provisional serotypes be admitted to the Shigella schema as S. boydii 16, 17, and 18.

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We conducted a prospective study of travelers' diarrhea on 73 physicians and 48 family members attending a medical congress in Mexico City, in October, 1974. Fecal and blood specimens were collected before, during and after their visit and examined for enteric bacterial pathogens, viruses and parasites. In 59 (49 per cent) participants travelers' diarrhea developed. Median duration of illness was five days. Onset occurred a median of six days after arrival. An etiologic agent was found in 63 per cent of ill participants. Enterotoxigenic Escherichia coli of different, non-"enteropathogenic" serotypes was the most common cause; other responsible pathogens included salmonellae, invasive Esch. coli., shigellae, Vibrio parahaemolyticus, Giardia lamblia and the human reovirus-like agent. Consumption of salads containing raw vegetables was associated with enterotoxigenic Esch. coli infection (P = 0.014). Travelers' diarrhea in Mexico is a syndrome caused by a variety of pathogens, the most common of which is enterotoxigenic Esch. col.

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A laboratory investigation was conducted on cultures collected from travelers before, during, and after a trip to Mexico to characterize the etiology of traveler's diarrhea. Four laboratory methods for detecting enterotoxigenicity of Escherichia coli were evaluated: the infant mouse assay, the Chinese hamster ovary (CHO) cell assay, the Y1 adrenal cell assay, and the rabbit ileal loop. Although a number of common enteric pathogens were identified as a cause of traveler's diarrhea, including six serotypes of Salmonella, two serotypes of Shigella, Vibrio parahaemolyticus, Giardia lamblia, and Entamoeba histolytica, enterotoxigenic Escherichia coli was most commonly isolated. Strains were identified that produced only heat-labile enterotoxin (LT), only heat-stable enterotoxin (ST), or both LT and ST. The infant mouse assay yielded results falling into two distinct groups, providing a clear separation of positive and negative cultures. The CHO assay also formed two groups, with positive cultures producing 11% or more of the elongated cells. There was good agreement between the CHO and the Y1 adrenal cell assays for detection of LT. The adrenal cell system for detection of LT was more suitable than the CHO assay for processing large numbers of specimens because of the miniculture modification of this method utilized in this study. The infant mouse method was a simple and reliable method for detecting ST.

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Five patients who developed acute watery diarrhoea while travelling in Mexico in October, 1974, were found to have enterotoxigenic Escherichia coli in their stool which produced heat-stable enterotoxin (S.T.) without producing heat-labile enterotoxin (L.T.). These S.T.-only E. coli, which have previously been described as causing diseases in animals, must now be regarded as pathogenic for humans as well.

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