large bombing raids, contributing to the shortage in hospital beds [9]. Furthermore, in Germany due to the increasing requirement to augment the labor force, TB patients were forced to work, thereby reducing any chance of recovery and accelerating their path to a fatal outcome. With only a few limitations, even patients with contagious TB were considered capable to work. Other inhumane measures of accelerating death included purposefully starving moribund patients and shortening the lives of so-called anti-social cases in selected TB hospitals, which often were combined with those for patients with psychiatric disorders [12].
Interestingly, the significant rise in TB mortality between 1937 and 1947 in Bavaria, which is illustrated in Figure 1, was almost completely due to pulmonary TB; by contrast there was only a small increase in extrapulmonary TB (Fig. 2), possibly due in part to unavailable or insufficient diagnostic methods. This phenomenon was also seen in other German provinces: pulmonary TB ranging from 91% of all TB deaths in Berlin down to 82% in Hesse in 1947. In the U.S. Zone, 85% of the mortality was ascribed to pulmonary TB and 15% to TB of other organs. These proportions are identical with the figures for all of Germany over the 3-year period, 1935–1937 [9]. That the rise of TB deaths was caused mainly by pulmonary TB was also observed in other countries (see chapters 6–19).
The data from Bavaria confirm that the TB mortality during wartime and at the end of the WWII was generally larger in the cities than in the rural districts, as shown on Figure 2.
Fig. 1. Tuberculosis mortality in Bavaria, Germany, 1937–1947, adapted from [13], with permission of Springer.
Fig. 2. Increase of TB mortality in Bavaria, Germany, at the end of WWII, mainly in cities compared to rural districts, adapted from Ref. [13], with permission of Springer.
One of the reasons for higher TB mortality rates in large cities (Fig. 3) may be owing to either the prevailing insufficient food supply (or to the better provision of food in rural areas). In Berlin, for example, food shortages were presumably enhanced because of the difficulty in procuring food from the surrounding farmland [14]. A further reason was presumably that living conditions were less crowded in rural areas [9]. An additional reason for the exacerbation of the prevalence of TB in big cities such as Berlin was the considerable loss of housing accommodations by massive allied bombing raids after 1943. Meyer mentions that in the different districts of Berlin between 25 and 50% of houses had been destroyed, heaviest in industrial districts where the lower social classes lived [14]. Virtually the same pattern of destruction occurred in England where industrial cities were the main target of German bomb and V2 attacks.
Rich versus Poor
Using available data from different parts of the city, Klesse [15] infers a steeper increase in TB mortality from 1939 to 1944 within Berlin districts predominantly inhabited by working class people compared to those where the more affluent preferred living. For instance, in the whole of Greater Berlin, TB mortality increased by 53% during this period, whereas in the Neukölln district it rose by 68%. Moreover, Neukölln was not among the poorer city areas; in fact, it was rather by averaging richer and poorer districts that Klesse concluded that some poorer districts had more TB than other more affluent ones. The same was true for Vienna, as mentioned by Daniels [3], where the highest TB mortality was in the working class boroughs (up to 322 per 100,000 inhabitants).
Fig. 3. TB mortality in selected European cities, 1938–1947, adapted from Ref. [3].
An interesting explanation for the faster elimination of infectious sources in the Soviet zone (GDR) during the first years after WWII in comparison with the western zones of Germany (FRG; Fig. 7 at the end of chapter 5 has been presented by Ferlinz et al.: the twofold higher TB mortality of infectious sources after the war – presumably due to the lack of TB drugs and the worse economic situation – reduced the spread of the TB bacilli to the population. Additional factors were the less favorable conditions in the FRG due to the substantially larger proportion of foreigners (immigrants as well as asylum seekers) from countries with high TB incidence [16].
Host-Dependent Risk Factors
Host-dependent factors are important conditions that weaken the immune defense system of the body. The defense mechanisms against M. tuberculosis are complex, a variety of factors are involved, from innate and adaptive cellular to humoral immune responses. If these are impaired, it increases TB morbidity, chiefly through increased progression from already present latent infection to active disease with accompanying mortality. Impaired immune defenses are an increasing cause of TB disease and death in developed as well as in underdeveloped countries.
While the risk of becoming infected with M. tuberculosis is largely exogenous in nature as described above, the risk subsequent to acquisition of latent infection with M. tuberculosis is largely endogenous [17]. Thus, crowded congregate settings are conducive to increase the probability of successful transmission of tubercle bacilli. While infection with M. tuberculosis is the necessary or initiating cause, some reduction in the body’s resistance, probably decreased cellular immunity, is undoubtedly the sufficient or promoting cause [18]. What we refer to here as host-dependent factors broadly circumscribes a multitude of factors that increase the risk of progression from latent infection with M. tuberculosis to overt clinical disease by putatively undermining cellular immune defenses [19]. Many of these factors are well established, leaving little doubt about their causal role in increasing the risk of progression to TB (such as diabetes mellitus, silicosis, immunosuppressive therapy with certain drug classes, etc.), while the relationship is causally less certain in others (such as gastrectomy, certain blood groups). One factor of major global implication because of its shear population magnitude is malnutrition or, more precisely, protein energy malnutrition.
Fig. 4. Tuberculosis