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SYNOPSIS. Monkey kidney cells (LLC‐MK2) grown in flasks and on coverslips in Leighton tubes were used as host cells for the growth of the intracellular stage, Leishman‐Donovan bodies (LDs), of Leishmania donovani obtained from hamster spleen. These parasitized cultures were then used to determine the ability of acriflavin to induce dyskinetoplastic LDs. LD‐infected cells were somewhat fewer in number than uninfected cells at all times except for the 1st day after infection. The parasites attained their maximum numbers on the 5th day after infection of the cultures having a 1.9‐fold increase at that time. When acriflavin was added to the cell culture medium (250 mμ/ml) the numbers of monkey kidney cells did not differ greatly from non‐treated cultures until 6–7 days after treatment with acriflavin. Similarly, the numbers of LDs in acriflavin‐treated cell cultures, altho somewhat below those of untreated cultures, did not differ greatly from them. The combined effect of acriflavin and LDs reduced the numbers of monkey kidney cells in treated, LD‐infected cell cultures more than either alone. Dyskinetoplastic LDs appeared in considerable numbers in acriflavin‐treated, LD‐infected cell cultures. Dyskinetoplastic and normal LDs harvested from cell cultures were inoculated into NIH medium and incubated at 27 C for transformation into leptomonads. There was no indication that dyskinetoplastic LDs were capable of transforming into leptomonads.
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Robert Herman (1968) studied this question.
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