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Was Historical Plague a Viral Or Bacterial Disease? the Question of Immunity

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Was Historical Plague a Viral Or Bacterial Disease? the Question of Immunity CHAPTER SIX WAS HISTORICAL PLAGUE A VIRAL OR BACTERIAL DISEASE? THE QUESTION OF IMMUNITY Introduction Cohn and Scott and Duncan advocate alternative theories to the eff ect that historical plague was a viral disease and maintain, in accordance with this view, that survival of plague infection provided persistent and strong immunity. As a rule, bacterial diseases confer only modest and transient immunity in survivors who therefore may repeatedly fall ill from the same bacterial diseases; it is viral diseases such as small pox, chicken pox, measles and mumps that produce persistent and strong immunity in survivors. Most medical authorities on plague who had the opportunity of observing large plague epidemics in the fi rst dec- ades of the twentieth century agree that survival of plague infection conferred only weak and transient immunity (see below).1 If the obser- vation or assertion were correct that survivors of historical plague dis- ease acquired strong and persistent immunity, it would constitute substantial evidence that historical plague epidemics could not have been bubonic plague or indeed any other bacterial disease, and proba- bly was a viral disease instead. Since this type of assertion, like the assertions on the manifestations of plague discussed above, tend to fal- sify the bubonic plague theory and to justify the search for a tenable alternative, this subject of immunity must also be examined suffi ciently thoroughly to decide the matter. Twigg, who advocates a bacterial alternative, has not recognized that there is such a problem and does not discuss it, which in itself can be taken as an indication of the weak- ness of this case. Th eoretically, a dangerous epidemic disease producing high mor- bidity and lethality rates can produce a violent reduction of a popula- tion, but some essential distinctions must be made. Diseases producing strong and persistent immunity in survivors are characterized by strong 1 Benedictow 1993/1996: 126–30. O. Benedictow - 9789004193918 Downloaded from Brill.com09/26/2021 05:56:37PM via free access 206 chapter six limitations with respect to possible long-term demographic eff ects. In naïve populations (i.e. populations without prior experience with the disease) exceeding 500,000 to one million persons, aft er a fi rst onslaught which may be dramatic, such diseases will recur in the constituent local societies normally in a fi ve to ten year cycle, in the meantime circulat- ing elsewhere. Th is is the period needed to bring into existence suffi - cient numbers of interacting persons without previous infectious experience with these pathogens to allow rise of epidemic spread among them (as distinct from endemic spread). In other words, in ordinary populations there must have come into being a suffi cient number of susceptible children to assure that each case of an epidemic disease will be transmitted to at least one other child or susceptible person,2 otherwise no epidemic will arise and the disease’s presence will take on an endemic (sporadic) pattern or disappear. Th e older populace will contain too large proportions of resistant survivors to be much involved in the epidemic. In the typical mortality pattern of, e.g., smallpox, the rate of mortality in no age group older than 5–10 years amounts to even one-fi ft h the rate in the age group 0–5 years.3 Even smallpox, which is characterized by high virulence and extraordinary powers of spread, will therefore normally produce modest general mortality rates in populations where adult generations have previous infectious experience with the disease. Scott and Duncan correctly point out that recovered “persons were immune to the smallpox virus for a long time so that each new epidemic swept with high infectivity through only the children who had been born in the interim, of whom about 20% died […].”4 Th is corresponds to a rate of population mortal- ity of a few per cent, which does not prevent local or regional societies from rapidly recuperating their demographic strength and producing population growth between epidemic outbreaks, so that this epidemic pattern is compatible with long-term population growth. Th is is a specifi c refl ection of a general pattern which ensures that, in substantial populations, recurrence of acute infectious diseases which produce strong and persistent immunity in survivors will nor- mally have quite limited demographic eff ects over quite short periods. In order to cause a large-scale and protracted diminution of the 2 Cf. Scott and Duncan 2001: 37–8. 3 Greenwood 1935: 240. 4 Scott and Duncan 2001: 376. O. Benedictow - 9789004193918 Downloaded from Brill.com09/26/2021 05:56:37PM via free access was historical plague a viral or bacterial disease? 207 population like those witnessed in Europe in the late medieval period, a disease must display a pattern of dramatic recurrence, sparing no substantial sections of the populations. Obviously, epidemic diseases which do not produce good persistent immunity in survivors will have much larger powers of spread, recurrence and mortality than diseases conferring persistent immunity. Consequently, other factors being equal, they will also tend to produce much higher mortality rates over time, since the whole population will be at risk every time they recur. Th is is therefore a question of considerable epidemiological and demo- graphic importance which will have to be suffi ciently discussed to reach a certain conclusion. Th e analysis above reveals that failure to produce strong and persistent immunity in survivors is an essential property for a disease if it is to function as a causal explanation for the type of demo- graphic developments which took place in the Late Middle Ages. Th us, epidemiological theory militates against the notion that the Black Death and subsequent plague epidemics could have been a viral dis- ease but is compatible with a bacterial disease. Nonetheless, Cohn argues that historical plague epidemics aft er the Black Death assumed the character of a child disease, and that this shows that historical plague was a viral disease conferring persistent immunity on survivors, a position that will be discussed below. Scott and Duncan, who also maintain that historical plague was a viral disease that should, accordingly, produce immunity in survivors, conspicuously refrain from addressing this question in a focused or systematic way, since children are strongly underrepresented in regis- tered cases of fi loviridal diseases, represented by Ebola disease and Marburg disease.5 At various places in their monograph they present a number of purported instances of possibly increased resistance or immunity in persons or populations which have in common that they do not constitute valid material for tenable inference—what they present is speculation without a fi rm evidential basis.6 Although Scott and Duncan combine the professions of demogra- pher and biologist, they do not discern between incidence as related to degree of risk of exposure to infection and susceptibility. Th ey assert that Pollitzer should have maintained that “adolescents and adults aged 5 Khan 2003: 1167. 6 Scott and Duncan 2001: (104), 121, 139, 145, 155, 205, 232, 281–2, 329, 355–6, 377–8, cf. Index under immunity. O. Benedictow - 9789004193918 Downloaded from Brill.com09/26/2021 05:56:37PM via free access 208 chapter six up to 45 years displayed the greater susceptibility.”7 However, Pollitzer states that “according to most observers” “the incidence of bubonic plague was highest in adolescents and in adults up to the age of about 45 years” which is certainly a very diff erent opinion.8 It is, therefore, important to note Wu Lien-Teh’s general statement on the matter: “Most investigators are agreed that, on the whole, diff erences in the age, sex, racial and also occupational incidence of bubonic plague are due to diff erences in exposure to infection as brought about by varying modes of life and not to intrinsic causes.”9 Pollitzer supports this posi- tion unequivocally when he paraphrases it quite closely: “Most workers are agreed that diff erences in the race and sex incidence of bubonic plague cases, as well as […] among certain occupational groups […] are due merely to diff erences in the degree of exposure of the various groups to the infection and not to intrinsic causes.”10 “Diff erences in the degree of exposure of the various groups to the infection” is a key phrase. Too oft en it is forgotten that epidemic appear- ances can be deceptive, because social conditions can systematically aff ect the intensity of the infective process in relation to particular social groups according to the distributive functions of relative risk of exposure. In this context it must be emphasized that this occurs in ways that mimic the workings of acquired diff erences in immunity. As explained above,11 at the heart of the matter is the fact that epidemiol- ogy is fundamentally a subdiscipline of sociology, and attempts to explain how various social conditions and patterns of behaviour aff ect the probability of contagion being transmitted to human beings or between human beings in a population of susceptible people. In short, age-specifi c role-patterns may produce particular risks of exposure and age-specifi c patterns of morbidity and lethality. Th is is the essence of Wu Lien-Teh’s and Pollitzer’s statements on the matter. Likewise, changes in mortality rates cannot be taken as evidence of increasing immunity or resistance in a population as Cohn and Scott and Duncan argue. It is important to take into account the fact that human understanding of the contagious nature of epidemic disease may lead to changes in individual behaviour and the implementation 7 Scott and Duncan 2001: 139. 8 Pollitzer 1954: 504. 9 Wu Lien-Teh 1936c: 399.
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