RESUMO
Background@#Line probe assay (LPA) is standard diagnostic tool to detect multidrug resistant tuberculosis. Noninterpretable (NI) results in LPA (complete missing or light wild-type 3 and 8 bands with no mutation band in rpoB gene region) poses a diagnostic challenge. @*Methods@#Sputum samples obtained between October 2016 and July 2017 at the Intermediate Reference Laboratory, All India Institute of Medical Sciences Hospital, New Delhi, India were screened. Smear-positive and smear-negative culturepositive specimens were subjected to LPA Genotype MTBDRplus Ver 2.0. Smear-negative with culture-negative and culture contamination were excluded. LPA NI samples were subjected to phenotypic drug susceptibility testing (pDST) using MGIT-960 and sequencing. @*Results@#A total of 1,614 sputum specimens were screened and 1,340 were included for the study (smear-positive [n=1,188] and smear-negative culture-positive [n=152]). LPA demonstrated 1,306 (97.5%) valid results with TUB (Mycobacterium tuberculosis) band, 24 (1.8%) NI, three (0.2%) valid results without TUB band, and seven (0.5%) invalid results. Among the NI results, 22 isolates (91.7%) were found to be rifampicin (RIF) resistant and two (8.3%) were RIF sensitive in the pDST. Sequencing revealed that rpoB mutations were noted in all 22 cases with RIF resistance, whereas the remaining two cases had wild-type strains. Of the 22 cases with rpoB mutations, the most frequent mutation was S531W (n=10, 45.5%), followed by S531F (n=6, 27.2%), L530P (n=2, 9.1%), A532V (n=2, 9.1%), and L533P (n=2, 9.1%). @*Conclusion@#The present study showed that the results of the Genotype MTBDRplus assay were NI in a small proportion of isolates. pDST and rpoB sequencing were useful in elucidating the cause and clinical meaning of the NI results.
RESUMO
The present study was designed to develop suitable biochemical markers of chronic dichlorvos exposure using rat as the animal model. Animals were exposed to dichlorvos (6 mg kg-1 (body weight) day-1) for 8 weeks and the activities of five potential markers were assayed. Acetylcholinesterase, assayed as an index of cholinergic function, was found to decrease in both haemolysate and brain tissue. Cytochrome oxidase, used as a marker of impaired energy metabolism, was also seen to decrease in platelets and brains of dichlorvos-treated animals. However, acid phosphatase, a lysosomal marker of tissue injury, was increased in both serum and brains of experimental animals. Chronic dichlorvos exposure also led to a decrease in the activity of glucose-6-phosphate dehydrogenase, which was assayed in brain as an index of oxidative stress. Dichlorvos administration did not affect 2', 3'-cyclic nucleotide phosphohydrolase. The present study therefore, indicates that apart from acetylcholinesterase, which is probably a non-specific marker of dichlorvos neurotoxicity, the levels of cytochrome oxidase, acid phosphatase and glucose-6-phosphate dehydrogenase may serve as useful determinants of dichlorvosinduced neuronal injury.
