Armstrong’s survey has also thrown some light on the effect of the influenza on previously tubercularized individuals. In a survey of 700 individuals who had had the acute disease there were ten arrested cases of tuberculosis, or 1.4 per cent. All these had been known to be arrested cases previous to the epidemic, and in none of them did the disease appear to have been actively and permanently lighted up. Some had manifested a slight activity, but all seemed to be on the way to a rearrest of the disease. On the other hand, thirteen cases, or 2 per cent. of the 700, were found to have active tuberculosis which had hitherto been undiagnosed, and an additional eight cases, with indefinite broncho-pulmonary signs, were designated as incipient tuberculosis cases. This is to be contrasted with an incidence of active tuberculosis in the pre-epidemic examination of approximately one per cent. These figures would indicate an increase in tuberculosis incidence. How may this be explained? The accuracy of these results will depend on how the 700 cases were selected. If, for example, individuals who feared tuberculosis because of known exposure, requested examination, the results might be influenced by their inclusion.
It has long been known that individuals with measles will not react to tuberculin tests, even though they have been positive before developing the measles, and though they will become positive again after recovery. The same may be said of vaccination. Individuals vaccinated against smallpox, who have measles, and are during their illness revaccinated, will not show an immediate reaction. The test will remain entirely negative, while after recovery, the immediate reaction may be obtained. Normally, it will appear in 95 per cent. of cases, while among those with measles the phenomenon remains absent in 90 per cent. The same phenomenon is present in certain other acute illnesses, particularly scarlet fever. It has been variously explained. von Pirquet, who was the first to observe it in measles, believed that the acute disease created a temporary inability to produce antibodies, and therefore designated the condition by the name “anergie.” The same phenomenon of anergie has been found recently to hold in the case of influenza. Debré and Jacquet, Lereboullet, Bloomfield and Mateer, as well as Berliner and Schiffer, have brought forth abundant evidence to this effect, following the 1918 pandemic. It has also been shown by Cayrel and others that there is a diminution of typhoid agglutinins in the serum of influenza patients vaccinated against typhoid. The agglutinin titer again increases after recovery. It is true that the agglutinin titer is not a measure of immunity, but it is frequently used as such and serves to give us some information on the subject. If, then, influenza is an anergic disease, a “maladie anergisante,” we have a theoretical explanation of the increase in severity of tuberculosis following the acute infection. We have long observed that tuberculosis frequently follows measles. We have recently been thoroughly convinced that influenza lessens resistance to secondary infection with streptococcus, pneumococcus, and other respiratory tract organisms. Shall the tubercle bacillus be added to this list? During the 1918 epidemic we saw men in the army camps who passed through an attack of influenza-pneumonia and died within a few weeks from tuberculous pneumonia or miliary tuberculosis. These men had previously been so free from signs of their tuberculosis, as to be accepted for military service as healthy individuals. The number of these cases was small, to be sure, but sufficiently large to convince us that there do exist instances in which tuberculosis is tremendously fired by an intercurrent influenza.
If we may judge merely by the balance of evidence and risk any conclusions from such conflicting testimony, we may sum up as follows:
1. Great variation in the interaction of tuberculosis and influenza must be expected, because of the many stages at which the tuberculous may be attacked, because of the altered mode of living of known consumptives, and because of the protected life of most of them.
2. Phthisical patients as a group, may be relatively insusceptible to influenza infection. This may be due to the tuberculous process itself or to some extrinsic, but nearly related cause.
3. But many individuals with pulmonary tuberculosis do get influenza.
4. And the disease, having been contracted, in many cases hastens the fatal termination of the tuberculous process.
5. It may be that this phthisical exacerbation occurs more frequently in individuals with latent tuberculosis, individuals who are not at the time mobilizing their protective antibodies.
Other infectious diseases.—We have found diversity of opinion regarding the relationship between influenza and tuberculosis, and yet the latter, being as a rule very chronic and presenting very definite signs which may easily be followed, should theoretically be a disease in which the results of study would be quite definite. When it comes to a study of other maladies we find the same difference of opinion frequently present.
It has been the experience of many that during influenza epidemics other acute specific infectious diseases appear to diminish, both in number of cases and in extent. At Camp Sevier, for example, two measles wards had been quite constantly full of patients up to the time of the fall influenza epidemic, while during the time of the epidemic one ward appeared sufficient to hold all cases of measles. In the stress of the epidemic this difference was probably more apparent than real, and certainly is not to be taken as of statistical value.