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Glycolipids belonging to the family of acylated trehaloses were isolated from Mycobacterium fortuitum, a rapidly growing mycobacterial species, and tested in the serologic diagnosis of human pulmonary tuberculosis by enzyme-linked immunosorbent assay. Di- and tri-O-acylated trehaloses from M. fortuitum reacted with serum antibodies of patients with pulmonary tuberculosis at higher titers than did with sera from healthy donors. With both glycolipids, the sensitivity of the test was above 0.80 at a chosen specificity of 0.98. Individuals with treated tuberculosis showed lower antibody titers compared with their initial reactivities. These data show that M. fortuitum could be used as a surrogate source of antigens for tuberculosis serodiagnosis.

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Blood adenine nucleotides were determined in patients with alcoholic and non-alcoholic liver diseases. They included patients with alcoholic hepatitis (AH), alcoholic liver cirrhosis (ALC), non-alcoholic liver cirrhosis (NALC), and amoebic liver abscess (ALA) (28 patients). A decrease of 28% to 39% in blood ATP levels was observed among the patients with AH and the cirrhotic groups, respectively (p less than 0.05), whereas no significant changes in blood ATP levels were detected in the ALA group. Although total blood adenine nucleotides were significantly diminished in AH, ALC, and NALC groups, the AH patients retained their energy relationships within normal range. On the other hand, the cirrhotic groups, independently of their etiology, failed to maintain an adequate ATP/ADP ratio, energy charge, and phosphorylation potential in the blood, suggesting a decreased energy availability in their blood cells. Nevertheless, the mechanism involved in these effects remains to be elucidated, a failure of the damaged liver to supply purines to extra-hepatic tissues might be a major event altering the blood energy parameters.

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This investigation sought to determine whether detection of salivary IgA antibodies to Entamoeba histolytica could identify intestinal amebic infections among 223 school children. Four groups of children were identified through coproparasitoscopic examination: E. histolytica as other parasites only (20%); and parasite-free (25%). The diagnostic accuracy of salivary IgA antibodies to an E. histolytica membrane extract was 91.5% (sensitivity, 85%; specificity, 98%), maintaining high predictive value at different prevalences. Also, a positive correlation (r = .753, P less than .001) was observed between fecal E. histolytica membrane antigen levels and salivary IgA antibody activity. Measurement of IgA antibodies in saliva may be useful in diagnosing intestinal infections with E. histolytica within a wide range of prevalences. Moreover, sampling of saliva may be a useful non invasive test for immunoepidemiologic surveys.

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The clinical utility of an ELISA test with monoclonal antibodies to detect antigen of Entamoeba histolytica in feces was evaluated in 150 patients with gastrointestinal symptoms. Each subject was examined by rectosigmoidoscopy with rectal smear and/or a triple stool search for ova-bacteria-parasite (OBP); in addition, one stool sample was collected for the ELISA test. All the tests were independent and double blind. E. histolytica was detected by OBP and/or rectosigmoidoscopy in 66 patients; 61 patients had other parasites; and in 23, no parasites were identified. Of all patients, 116 were positive for the ELISA test. Of these, E. histolytica was identified in 52. In 47, other parasites were identified and in 17, no parasites were found. The ELISA test with a monoclonal antibody against E. histolytica antigen showed higher sensitivity than the standard diagnostic methods: the ability to detect the presence of E. histolytica antigen regardless of the destruction of the parasite or of the error due to misidentification of the parasite resulting from faulty preparation of the samples.

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Adenosine administration delayed the fatty liver and cell necrosis induced by carbon tetrachloride without affecting the action of the hepatotoxin on protein synthesis and liver triacylglycerol release. Adenosine produced a drastic antilipolytic effect accompanied by a decrease in the incorporation of [1-14C]palmitic acid into triacylglycerols and free fatty acids of the liver. Furthermore, a decrease in the serum levels of ketone bodies was observed at early times. The nucleoside also avoided the release of intracellular enzymes and prevented the lipid peroxidation produced by carbon tetrachloride during the 4 hr of treatment. The protective action of adenosine was transient, lasting 3-4 hr, probably the time required to be metabolized. The results suggest that the antilipolytic effect of the nucleoside, the inhibition of hepatic fatty acid metabolism, and the decrease in carbon tetrachloride-induced lipoperoxidation that it produced are involved in the delayed acute hepatotoxicity induced by carbon tetrachloride.

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The role of adenosine as a possible physiological modulator was explored by measuring its concentration in different tissues during a 24-hour period. Initially the circadian variations of adenosine and other purine compounds such as inosine, hypoxanthine, uric acid and adenine nucleotides were studied in the rat blood. A daily cyclic response was observed, with low levels of adenosine from 08.00 - 20.00 h, followed by an increase from this time on. Inosine and hypoxanthine levels were elevated during the day and low at night. The uric acid changes observed indicate that the decrease in purine catabolism coincides with a decrease in inosine and hypoxanthine levels and an increase in adenosine. The blood adenine nucleotides, energy charge and phosphorylation potential remained constant during the day and showed oscillatory changes during the night. Similar studies were made in the liver, a primary source of circulating purines. Liver adenosine was high during the night while inosine and hypoxanthine remained low along the 24 hours. The results suggest that liver purine metabolism might participate in the maintenance and renewal of the blood purine pool and in the energy state of erythrocytes in vivo.

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