Future of Infectious and Malignant Diseases 
greater understanding of the natural history of the disease in man, 
the causative organisms—their mode of transmission, adapta- 
bility, mechanisms for persistence inside and outside the host—et 
cetera. It appears likely that eradication will depend more upon 
knowledge of such factors than upon proficiency in the diagnosis 
and therapy of individual patients with tuberculosis.” 
This statement can also be applied to any eradication pro- 
gramme planned for infections other than tuberculosis. By 
now it should be abundantly clear to everybody that even 
individual therapy rarely, if ever, ““eradicates’’ the infectious 
agent from the organism of the treated individuals. If this con- 
cept is extended to the population at large, it may lead only to 
an alarming increase in the number of drug-resistant persisters 
which would be driven underground where they cannot be 
detected. Such micro-organisms could strike at any time and, in 
the absence of new and effective therapeutic measures, could 
cause havoc among the susceptible population. 
Penicillin has been used for the rapid treatment of gonorrhoea 
for the past twenty years, and yet the disease has rapidly 
increased during the past eight years in the 12-23-year age 
group. Although this increase in the incidence of infection is 
caused chiefly by the awareness of availability of an effective 
therapy and a disregard for any other “safety measure’’, it 
recently became known that gonococcal infection of the female 
genito-urinary tract can probably never be “‘eradicated”’ even 
during an intensive course of individual therapy, because of 
changes in bacterial cell metabolism which may be responsible 
for relative insusceptibility to antibiotics. 
Development of drug-resistant mutants has been observed 
repeatedly in connexion with the notorious infection by staphy- 
lococci in hospitals. Drug resistance as a function of time in 
tuberculosis infection has been described by Stead as follows 
(Fig. 1). A young adult who, let us say in 1953, showed first 
signs of active tuberculosis in the upper lobe of his lung in the 
presence of fibrotic and calcified lesions of the middle lobe 
representing primary infection, may have been treated inade- 
quately. A child exposed to contact with him in 1953 would be 
EOo 
