Biomedical subjects
Publications and source records attributed to W H Hall.
Asparagine supplies not only nitrogen but also carbon to growing cells of Myobacterium tuberculosis. The carbon of asparagine is rapidly taken up and extensively utilized.
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Acidic phospholipids neutralized the antistaphylococcal activity of rabbit, human, and rat serum and purified rabbit beta-lysin as well. Several tissue bactericidal factors and cationic antibiotics were also neutralized. The neutralizing ability of all anionic lipids tested, together with the lack of this ability for the electrostatically neutral phosphatidylcholine, suggested that neutralization resulted from formation of electrostatic complexes between negative charges on the lipids and positive charges on the bactericidal substances. The neutralization of these host defense systems by phospholipids can explain the ability of phospholipids to increase bacterial virulence.
(14)C-isoniazid (INH) was used to study the relationship between drug uptake or binding by Mycobacterium tuberculosis and growth inhibition of the organism, which is dependent upon the concentration of drug and the duration of exposure. When strain H37R(a), grown in modified Sauton's liquid medium, was treated with 0.1 mug of INH per ml for 2 to 6 hr, followed by 10 mug of nicotinic hydrazide (NH) per ml to block further INH uptake, growth was retarded but not completely inhibited upon continued incubation. NH itself did not retard growth. However, cells treated in a similar manner with INH alone grew normally when diluted 1:100 in fresh, drug-free media. Uptake data showed that bacilli exposed to 0.1 mug of INH per ml accumulated 5.5, 9.7, and 12 mmug/mg of dry cells at 2, 4, and 6 hr, respectively. Other experiments suggested that once isoniazid is bound, it is not rapidly lost when NH is added or when the cells are diluted in fresh media. In the presence of 1.0 mug of INH per ml, tubercle bacilli took up 10 to 37 mmug/mg of dry cells in 20 to 90 min. These cells were not markedly inhibited when diluted 1:40 in fresh NH-containing media and incubated for 6 days. Growth inhibition of tubercle bacilli by INH depends on the uptake of sufficient drug, but the evidence obtained in this study suggests that the absolute concentration of bound INH is not as important in the action of the drug as is the maintenance of a critical cellular concentration for a requisite period of time.
A photometric method was used to measure the bactericidal kinetics for Brucella abortus of freshly drawn rabbit blood during the time before clotting. This antibrucellar activity varied between rabbits in different immunologic states. Nonimmunized rabbits had moderate bactericidal activity after a lag of about 2 min. The blood of some immunized rabbits gave an immediate and strong kill, but in certain other immunized rabbits, especially when hyperimmunized, the bactericidal activity was inhibited. It appeared that serum bactericidins and complement are sometimes as active in unclotted blood as they are in serum. However, this bactericidal activity can be either increased or neutralized by immunization. The prozone bactericidal inhibition phenomenon (Neisser-Wechsberg) found in immune serum may, in fact, reflect inhibition taking place in vivo. Inhibition of the bactericidal activity in blood can contribute to the persistence of chronic infections and individual variations in resistance.
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Washed-cell preparations of Mycobacterium tuberculosis strain H37Ra and M. smegmatis 607 grown in Sauton's medium demonstrated a lag in glutamate oxidation. Washed-cell preparations of M. fortuitum and M. phlei oxidized glutamate immediately and in a linear fashion. Glutamate was oxidized without a lag by washed cells of M. tuberculosis H37Ra and M. smegmatis 607 harvested from a modified medium containing glutamate. Chloramphenicol inhibited the oxidation of glutamate by washed cells grown in the absence of glutamate. These findings suggested the induction of either an enzyme system for glutamate oxidation or a glutamate transport system. The activity of glutamic dehydrogenase was not significantly greater in extracts prepared from cells grown with glutamate. However, the initial rate of glutamate uptake by induced cells was three to four times higher than in noninduced cells. The induction of the glutamate transport system in M. tuberculosis H37Ra and M. smegmatis 607 was shown to parallel the induction of glutamate oxidation. After a 60-min lag, the inducible glutamate transport system appeared. Chloramphenicol prevented the induction of glutamate uptake, although the antibiotic had no effect on glutamate uptake by previously induced cells. Some of the properties of this glutamate uptake system are described.
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