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Variations in natural resistance to tuberculosis

Published online by Cambridge University Press:  15 May 2009

David F. Gray ,
Heather Graham-Smith  and
John L. Noble
David F. Gray
Affiliation:
From the School of Bacteriology, University of Melbourne, Parkville N. 2, Victoria, Australia
Heather Graham-Smith
Affiliation:
From the School of Bacteriology, University of Melbourne, Parkville N. 2, Victoria, Australia
John L. Noble
Affiliation:
From the School of Bacteriology, University of Melbourne, Parkville N. 2, Victoria, Australia
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1. ‘Resistant’ and ‘susceptible’ species of animals appear to be more or less equally susceptible to lung infection with equal doses of tubercle bacilli. Therefore it is pertinent to ask whether recognized natural differences in species resistant are in fact significant. For example, in terms of death rates (i.e. of overall resistance) the C57 mouse is at least as susceptible to tuberculosis as the guinea-pig and much more so than man.

2. Resistant, moderately susceptible and susceptible strains of mice as determined by death rates when exposed to large infecting doses, were equally susceptible to intranasal infection with small numbers of tubercle bacilli.

3. A state of tolerance of the parasite by the host lasting for about 3 weeks was observed in all mouse strains, regardless of ultimate strain resistance.

4. Pre-allergic deaths commenced in all groups when the tuberculous processes left insufficient normal lung to support life, but the deaths stopped first in the resistant strain and last in the susceptible strain, coinciding approximately in each strain with the onset of allergy.

5. Acquired immunity, once established, appeared not to vary in quality from one mouse strain to another, at least during 3 months' observation.

6. Racial or strain variations in the resistance of mice to tuberculosis are therefore natural, only in the sense that speed of onset of acquired immunity is probably genetically determined for each strain.

7. It is suggested that both species and racial variations in natural resistance to pulmonary infection are insignificant. Differences in the subsequent course of the disease appear to be explainable by the rapidity, efficiency and duration of the acquired immune response.

Type
Research Article
Information
Journal of Hygiene , Volume 58 , Issue 2 , June 1960 , pp. 215 - 227
Copyright
Copyright © Cambridge University Press 1960

References

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