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Partitioned between aqueous methanol and petroleum ether, the unsaponifiable pigments of Mycobacterium kansasiiwere all epiphasic. Thin-layer chromatography of these carotenoids showed that M. kansasiiformed at least nine pigments. These pigments were identified by their chromatographic properties and spectral characteristics as phytoene, ζ-carotene, neurosporene, lycopene, leprotene, γ-carotene, δ-carotene, α-carotene, and β-carotene. Three additional pigmented spots on thin-layer chromatography found in trace amounts were possibly degradation products of the major carotenoids.

This report deals with the differential diagnosis between Mycobacterium marinumand M. kansasii.We found that the two species could be differentiated by using six main tests, namely, the nitrate reduction test, the arylsulfatase test, the ability to grow in the presence of 10.0 μg of amithiazone per ml, the ability to grow in the presence of 5.0 μg of kanamycin per ml, the temperature-ratio test, and the rate of growth on solid medium. In contrast to M. kansasii, considerable variation was observed among strains of M. marinum.However, the evidence obtained was not considered sufficient to justify the conclusion that more than one species was represented among the strains identified as M. marinum.

The fluctuation test shows that Mycobacterium tuberculosismutates to resistance to isoniazid, streptomycin, ethambutol and rifampin spontaneously and at random. The average mutation rates for the drugs, in the same order, were calculated to be 2.56 × 10−8, 2.95 × 10−8, 10−7, and 2.25 × 10−10mutation per bacterium per generation. The relatively high mutation rate to ethambutol resistance and the low mutation rate to rifampin resistance were confirmed by analyzing the increase in the proportion of mutants with time in a growing population of the tubercle bacilli. The highest proportions of mutants to be expected in unselected populations of the tubercle bacilli were calculated from the results of fluctuation tests.

A single transport system was found to accumulate l- and d-alanine, glycine and d-serine in Mycobacterium tuberculosis.The results of inhibition experiments suggested that the antibiotics d-cycloserine and O-carbamyl-d-serine were also transported by the alanine-glycine-d-serine system. A d-cycloserine-resistant permease-competent (d-CSr/perm+) mutant and a d-cycloserine-resistant permease-defective (d-CSr/perm−) mutant were isolated. The d-CSr/perm−mutant was not found to be more resistant to the drug than was the d-CSr/perm+mutant. The data were consistent with the conclusion that resistance to d-cycloserine in the tubercle bacilli is primarily due to mutations in the gene(s) controlling the enzyme d-alanyl-d-alanine synthetase. The mutation rate was calculated to be about 10−10mutations per bacterium per generation.