The “Globalization” of Disease? India and the Plague*

i. j. cat a n ac hUniversity of Canterbury

In the sphere of disease, so it often seems, “globalization” began rela-tively early. According to Emmanuel Le Roy Ladurie, the first “par-

oxysm” of the “microbian unification of the world” occurred betweenabout 1300 and 1650.1 This was the era of the plague of the BlackDeath; the era, too, of the catastrophically rapid spread of smallpox,measles, and syphilis over much of the known world. A growth inhuman movement, through conquest, trade and travel, is seen as thekey factor in this process.

A further “paroxysm” of disease occurred in the earlier nineteenthcentury, with the seeming bursting forth of cholera from its Indianhomeland; again, human journeyings came to be seen as a major rea-son for its spread. The pandemic influenza of 1918–19 followed in thewake of troop movements associated with the last months of WorldWar I; now, after a mid–twentieth-century period of inflated optimismresulting from the coming of antibiotics, we have renewed and grow-ing fears—in some quarters, anyway—about the possibilities of rapid

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* I. J. Catanach was formerly Reader in History in the University of Canterbury,Christchurch, New Zealand. An earlier version of this paper was presented to a session onthe “globalization of disease” at the Twelfth Conference of the Asian Studies Associationof Australia, Sydney, September 1998. The article owes much to the advice of ElisabethCarniel in Paris, Carney Fisher in Adelaide, Australia, Bob Pilgrim in Christchurch, andthe author’s molecular biologist son, Andrew. But the author—a mere historian—mustbear full responsibility for venturing into unfamiliar realms, and for the conclusionsreached.

1 Emmanuel Le Roy Ladurie, “A Concept: The Unification of the Globe by Disease.”In Le Roy Ladurie, The Mind and Method of the Historian (Brighton, 1981), pp. 28–83;William H. McNeill, Plagues and Peoples (Oxford, 1977).

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global transmission of epidemic disease. The world-wide reaction tothe outbreaks of what is now generally said to have been plague inIndia in 1994 reminds us that folk memories of the sudden spread ofdisease—from the Black Death onwards—are still, understandably,very powerful.2

At the very end of the nineteenth century, and in the early twen-tieth century, another series of outbursts of plague—first in China andHong Kong, then in India, and then sporadically elsewhere—for atime inspired similar fears. India, the most heavily affected country,probably lost at least twelve and a half million people from plague inthe years 1896–1918; more if the years of plague’s extended “decline”in India, up to and after the second world war, are taken into consid-eration.3

Much of our understanding, as historians, of the more scientificaspects of plague and its diffusion still tends to be derived from com-paratively early studies of this Indian experience—in particular, thereports of what is commonly called the Plague Research Commission,published between 1906 and 1914 in supplements to the Journal of

Hygiene.4 For example, not very many years ago Ole Benedictow toquite a large extent found in those reports a model of what plagueshould be like, a template against which to judge reports of “plague” inmedieval and early modern Europe.5 Benedictow’s work is extraordi-narily wide ranging; his Nordic case studies are meticulously argued.But, like many a writer on the subject, he assumes that the nature ofplague has been basically constant over long periods of time. This

2 I. J. Catanach, “Déjà Vu? Indian ‘Plague’: 1896 and 1994.” History Now 2 (1996):1–6.

3 On the social and political aspects of this visitation see David Arnold, Colonizing theBody: State Medicine and Epidemic Disease in Nineteenth-Century India (Berkeley, 1993), Ch.5; I. J. Catanach, “Plague and the Indian Village, 1896–1914,” in Rural India: Land, Powerand Society under British Rule, ed. Peter Robb (London, 1983), pp. 216–243; Catanach,“Poona Politicians and the Plague,” South Asia n.s. 7 (1984): 1–18; Catanach, “Plague andthe Tensions of Empire: India 1896–1918,” in Imperial Medicine and Indigenous Societies, ed.David Arnold (Manchester, 1988), pp. 149–171; Catanach, “‘Who are your leaders?’Plague, the Raj and the ‘communities’ in Bombay, 1896–1901 ,” in Society and Ideology:Essays in South Asian History Presented to Professor K. A. Ballhatchet, ed. Peter Robb (Delhi,1993), pp. 196–221; Rajnarayan Chandavarkar, “Plague panic and epidemic politics inIndia,” in Epidemics and Ideas: Essays on the Historical Perception of Pestilence, ed. TerenceRanger and Paul Slack (Cambridge, 1992), pp. 203–240.

4 Officially, the Working Commission appointed by the Advisory Committee for theInvestigation of Plague in India—the Committee being nominated by the Secretary ofState for India, the Royal Society, and the Lister Institute.

5 O. J. Benedictow, “Morbidity in Historical Plague Epidemics,” Population Studies 41(1987): 401–431; Ole Jorgen Benedictow, Plague in the Late Medieval Nordic Countries: Epi-demiological Studies (Oslo, 1992).

Catanach: The “Globalization” of Disease? India and the Plague 1 3 3

assumption may no longer be altogether viable. Indeed, even beforeBenedictow’s work began to appear in English, W. F. Bynum had tren-chantly criticized the “presentism” of “the assumption that plague infourteenth-century Europe should have behaved like plague in twen-tieth-century India.” 6

But such a critique has within it another assumption: that we reallyunderstand the nature of plague in late nineteenth-century and earlytwentieth-century India. This article suggests that it may still be pos-sible to obtain the occasional new clue about the disease from a re re a d-ing of some of the earliest reports of this Indian visitation—reports,that is, that predate the investigations of the Plague Research Com-mission. More emphatically, it is argued that the historian must takecognizance of ideas on the roles of fleas and rodents in the spread ofplague that have developed since 1906–14, especially, perhaps, thosethat have become of increased relevance as a result of the unexpected“return” of plague to India in 1994. It is asserted, finally, that we mustpay close attention to recent advances in the study of the nature of theplague pathogen itself. Notions originating to quite a considerableextent between 1906 and 1914 about the role of human beings in thes p read of plague—over India, over the world, and over the centuries—a re certainly not rejected outright. But they are, in some cases, queried.

* * *

What is this understanding of plague—its origin and its diffusion—that is largely derived from the experience of India in the early yearsof the twentieth century? It must be said first, emphatically, that suchan understanding is not unscientific. It comes from an era when whathas been described as the “laboratory revolution in medicine” was inits first full flight.7 So, the root cause of plague was seen as a bacillus,Pasteurella pestis—later called Yersinia pestis after Alexandre Yersin, itssupposed discoverer. Plague was seen—in its beginnings, but often toall intents and purposes only in its beginnings—as a disease of rod e n t s ,especially rats, and their fleas. Human plague, it was thought, brokeout when rats and their fleas were brought into contact with humanbeings. They were brought into contact at least in part because of thedirty ways of human beings: the “sanitarian” outlook of the nineteenth

6 W. F. Bynum, review of Graham Twigg, The Black Death: A Biological Reappraisal.Times Higher Education Supplement, 5 April 1985.

7 Andrew Cunningham and Perry Williams, eds. The Laboratory Revolution in Medicine(Cambridge, 1992).

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century, sometimes tinged with an element of racism when it came tothe tropics, to a considerable extent lived on—this in spite of someearly hints from Bombay (now Mumbai) that plague could be as muchat home in relatively “clean” living quarters as it was in slums.8 By the1920s it was largely agreed that plague was most frequently spread bythe movement of rats and their fleas—movement for which humanbeings, again, through trade and travel, were largely responsible. Tech-nological innovation, it came to be believed, had vastly increased thepossibilities of the diffusion of plague. The outbreak in Bombay in18 9 6, following closely on plague in Hong Kong, was seen as an indica-tion of the disease’s newfound ability to cross the oceans in steamships.And plague could also now cross extensive land areas in railway wag-ons, while continuing to move over shorter distances in more tradi-tional conveyances, such as local coastal craft and bullock carts (espe-cially those loaded with foodgrains). Cert a i n l y, it was believed, it couldsurvive in rat-infested grainstores. And it was largely agreed that, withfavorable temperatures, humidity, and other circumstances, plague-ridden rat fleas could survive for some time—up to fifty days accord i n gto some re p o rt s—without hosts; such fleas could, for example, travel inbundles of clothing, blankets, and the like.9 Humans, then, and theirtechnology, were seen as vital factors in the diffusion of plague—but,given time, d e t e rm i n a t i o n, a nd re s o u rc e s, humans could stop the spre a dof plague. It was an optimistic notion, appropriate to the age of the“laboratory revolution” as well as to an era when imperialism in thetropics was not yet in visible decline.

The most common form of human plague in India in the late nine-teenth and early twentieth centuries was, undoubtedly, bubonic plague.But there were cases of pneumonic plague in India at this time, espe-cially—perhaps significantly—in Bombay in the earliest stages of thevisitation.10 In 1910–11 , furthermore, there was an outbreak in Man-

8 Report of the Municipal Commissioner on the Plague in Bombay for the Year ending 31stMay 1899 (Bombay, 1899), p. 21.

9 F. N. White, “Twenty years of plague in India with special reference to the outbreakof 1917–18,” Indian Journal of Medical Research 6 (1918–19): 190–216; W. Glen Liston,“The Milroy Lectures on Plague,” British Medical Journal (1924): 900–3, 950–4, 997–1001.For a useful summary of many of the generally accepted views of the late 1970s see J.-N.Biraben and Jacques Le Goff, “The Plague in the Early Middle Ages,” in Biology of Man inHistory: Selections from the Annales: Economies, Sociétés, Civilisations, ed. Robert Forster andOrest Ranum, tr. Elborg Forster and Patricia M. Ranum (Baltimore, 1975), pp. 48–55 .

10 Evidence of Ismail Jan Mahomad, Indian Plague Commission, Minutes of Evidence III,British Parliamentary Papers [PP] 1900 (Cd. 141), xxxii; p. 33. The investigations of theIndian Plague Commission of 1898–1900 are to be distinguished from the reports—whichcertainly bear more of the marks of the “laboratory revolution”—of the Plague ResearchCommission of 1906–14.

Catanach: The “Globalization” of Disease? India and the Plague 1 3 5

churia of what was thought to be purely pneumonic plague.11 By theearlier 1920s it was agreed that pneumonic plague could be caughtfrom droplets from the coughs of people suffering from bubonic plague,or, as in Manchuria, that it could in some way be caught from animalssuffering from the disease—in the Manchurian case, through activitiesinvolved in trapping tarabagans (marmots). But at this time, it seemsfair to say, pneumonic plague was seen as something of an exceptionto the rule; bubonic plague was thought of as the norm.

For most of the twentieth century the consensus, as we have seen,was that plague had come to Bombay in 1896 with rats in the cargo ofa ship from Hong Kong. Alternative explanations of its appearance,some of which had been put forward in 1896 or the years immediatelyfollowing, were largely dismissed or forgotten. There had been, forexample, a good deal of early speculation that plague had traveled toBombay from the Himalayan foothills, where, it was thought, it hadlong been found. Another early theory was that plague had beenbrought to Bombay from “Turkish Arabia, or the littoral of the PersianG u l f .”1 2 On the other hand, Lieutenant-Colonel George Waters, of theIndian Medical Service, persisted in publicizing his theory that theBombay plague had in some way originated in Bombay itself: that, forexample, it was the result of miasmatic “emanations” from stores ofdecaying grain.13 Yet another popular theory in the early stages ofplague in India had been that the “germ” was somehow “in the soil.” Inplague-affected areas the ground needed to be “broken up” and disin-fected. One District Collector had told the Plague Commission in1898 that this notion was “the working theory on which the whole ofour operations has been based.”14 But such ideas had soon come to beseen, in many ways correctly, as relics of bygone and outdated systemsof thought.

It must be said plainly that of all the possible explanations of thecoming of plague to Bombay, that of a Hong Kong origin still seems byno means unlikely. Plague was certainly present in Canton and HongKong in 18 9 4; a few cases were re p o rted in Hong Kong in 18 9 5 a n d

11 Wu Lien-Teh, A Treatise on the Pneumonic Plague (Geneva, 1926), pp. 9–10.12 P. C. H. Snow, Report on the Outbreak of Bubonic Plague in Bombay, 1896–97 (Bom-

bay, 1897), pp. 1–2. The claim was repeated as late as 1907 in Bombay Municipality, Reportby J. A. Turner M.B., D.P.H. Executive Health Officer on History of Plague in Bombay from1896 to 1907 (Bombay, 1907), p. 1.

13 George Waters, “The Bombay Plague,” Indian Lancet (1 November 1896): 430–431;Waters, “Plague in Bombay,” Journal of the Anthropological Society of Bombay 5 (1901): 391.

14 E. L. Cappel, Collector, Dharwar, Indian Plague Commission, Minutes of Evidence I,PP 1900 (Cd. 139), xxx; p. 83.

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many more in 1896.15 (How plague got to the south coast of China is,of course, another matter: the theory of a Yunnan origin may be inneed of some revision.)16 Plague-ridden rats and their fleas undoubt-edly could have survived the comparatively brief voyage by steamshipfrom Hong Kong to Bombay, just as, so it is generally assumed, theywere soon to survive voyages between Bombay, or Hong Kong, andSydney and other parts of the world where plague broke out aroundthis time. Indeed the distinguishing feature of this so-called “pan-demic” has been said to have been its “oceanic” nature.17 (However adecade ago two students of the Sydney plague of the earliest years ofthe twentieth century concluded, intriguingly, that its origins were“still obscure.”)18

It must be granted, too, that plague was said to have occurred fir s tin Bombay, in dock areas where cargoes recently arrived from HongKong were stored, although one would like a little more inform a t i o non the arrival dates of ships.1 9 C e rt a i n l y, the great Belgian student ofthe biology and the long-term history of plague, R. Devignat, con-cluded in 1 9 5 1 that the Bombay plague and the South Chinese plaguew e re of the same v a r i é té, or biovar. Plague had three distinctive biovars,he thought. One, Antiqua, was re p resented by the Plague of Justinian:the biovar survived in the twentieth century in Central Asia and Cen-tral Africa. Remnants of the second biovar, Mediaevalis, the plague ofthe Black Death, were now found in Southeastern Russia and Kurd i s-tan. The third biovar, Orientalis, was the plague of the third or most

15 Carol Benedict, “Framing Plague in China’s Past.” In Remapping China: Fissures inHistorical Terrain, ed. Gail Hershatter, Emily Honig, Jonathan N. Lipman, and RandallStross (Stanford, 1996), p. 34.

16 Acceptance of the idea of a Yunnan origin is the basis of much of the argument ofCarol Benedict, Bubonic Plague in Nineteenth-century China (Stanford, 1996). But CarneyFisher, of the University of Adelaide, is working on a critique of this notion.

17 M. Baltazard, “Epidemiology of Plague,” World Health Organization Chronicle 14(1960): 425. It will be seen below that Baltazard—a person of considerable significance inFrench plague research in the 1950s—was skeptical of the importance of the rôle of humanbeings in the movement of plague on land, and in particular in rural areas. But he was notsimilarly skeptical about the importance of steamships—sailed by human beings for thepurposes of human trade and human transport—in the movement of plague across theoceans in the modern era.

18 Peter Curson and Kevin McCracken, Plague in Sydney: The History of an Epidemic(Kensington, New South Wales, 1989), p. 41.

19 Evidence of I. J. Mahomad, Plague Commission, Minutes of Evidence III, p. 33; see alsothe map at the end of Vol. I of these Minutes which shows the order in which buildings inMandvi Bandar, Bombay, were affected. W. J. Simpson, A Treatise on Plague . . . (Cam-bridge, 1905), p. 67, says that some of the earliest cases of plague in Bombay were “amongMoltanies [Multanis] who had dealings with China.”

Catanach: The “Globalization” of Disease? India and the Plague 1 3 7

recent “pandemic,” the plague that is commonly said to have bro k e nout in Canton and Hong Kong in 18 9 4 and in Bombay in 18 9 6.2 0

Devignat was writing shortly before the elucidation of the structureof DNA in 1953. Quite remarkably, a recent study of the genetic struc-ture of seventy strains of Y. pestis kept in the collection of the InstitutPasteur in Paris has confirmed many of Devignat’s assertions about thebiovars of plague.21 But there appears to be nothing in that study thatspecifically confirms a Hong Kong–Bombay link in the 1890s. The sys-tematic preservation of “isolates” from plague cases seems to havebegun only in the first decade of the twentieth century; one suspectsthat we will never be able to compare isolates dating back to the earli-est days of plague in both cities.22 It has to be said, too, that Devignatnot only thought that the plague of late nineteenth-century Bombaywas closely related to the Hong Kong plague but also believed that itwas essentially the same as the plague found in Garhwal and Kumaon,in the Himalayan foothills of North India, for at least a century and ahalf.23 But even in the early 1900s an intelligent member of the IndianMedical Service had claimed to find certain significant bacteriologicaldifferences between the plague of the Indian plains and hill plague.24

In 1960 M. Baltazard and M. Bahmanyar came to a similar conclusion(though not, it would appear, purely on bacteriological grounds).25

The fact was that, during the whole of the period between the Britishassumption of rule in the hills in the early nineteenth century and18 9 6, what was believed to be hill plague only once, and then only verybriefly, ventured into a few nearby towns in Rohilkhand, on the edgeof the plains.26 (The reason for this was possibly that in the nineteenthcentury most transport between the hills and the plains was by packanimals, and rat fleas apparently do not care for the smell of many such

20 R. Devignat, “Variétés de l’espèce Pasteurella pestis: Nouvelle hypothèse,” Bulletinof the World Health Organization 4 (1951): 247–261.

21 Annie Guiyoule, Elisabeth Carniel, et al., “Plague Pandemics Investigated by Ribo-typing of Yersinia pestis Strains,” Journal of Clinical Microbiology 32 (1994): 634–641.

22 For some hints as to other possible methods of investigating the assumed Hong Kong-Bombay link see the article by Drancourt and Aboudhram referred to in n. 49 below.

23 Devignat, “Variétés,” p. 253.24 J. Chaytor-White to Government, United Provinces, No. 822, 25 March 1902, U.P.

Sanitary Proceedings, June 1902, 10, Oriental and India Office Collections, British Library,London [OIOC].

25 M. Baltazard and M. Bahmanyar, “Recherches sur la Peste en Inde,” Bulletin of theWorld Health Organization 23 (1960): 210. Even these authors seem—in this article, any-way—uninfluenced by notions of DNA.

26 J. Chaytor-White to Government, U.P., No. 3169 of 11 August 1905, India HomeSanitary Proceedings, February 1906, 331/2, OIOC.

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creatures.)27 Recent analyses tend to assume that Indian hill plague—in the twentieth century, anyway—is linked to the plague of CentralAsia, that is, to Devignat’s biovar Antiqua, rather than to his biovarOrientalis.28

There are, in fact, several other possibilities, besides the HongKong origin theory and the Himalayan foothill origin theory, whichneed to be considered when we are examining the Bombay plague.

In 1 9 7 8 the population economist R. H. Cassen speculated—a d m i t-t e d l y m e rely in a rather skimpily documented aside— t h at “what impor-tantly arrived in Bombay in 1896” might not have been “so much theplague pathogen as [the flea] X. cheopis which spread to the focal areasand then gradually was replaced by his more congenial predeces-sors.”29 A search for the probable source of these most interestinghypotheses leads to the work of the geographer A. T. A. Learmonth inthe late 1950s,30 to the massive compilation by R. Pollitzer publishedin 1954,31 to a little-known paper by H. H. King and C. G. Panditwhich appeared in 1931,32 and to the studies on rat-fleas by L. FabianHirst, commencing in 1913 and culminating in a magisterial volume,The Conquest of Plague, published in 1953.33

It was Fabian Hirst who first demonstrated the importance in theepidemic of plague, which began in India in 1896, of the particular rat-flea mentioned by Cassen, Xenopsylla cheopis. Hirst believed that X.

cheopis was the dominant rat-flea in those areas of India affected byplague. He showed that another rat-flea, Xenopsylla astia, was not aseffective a vector for plague as was X. cheopis. Xenopsylla astia was thedominant rat-flea in much of the south and east of India—this was themain reason, according to Hirst, for the comparatively small numberof plague cases in those parts of the country.

King and Pandit took Hirst’s argument a stage further. Xenopsylla

27 Including, it has been claimed, camels: Biraben and Le Goff, “The Plague in theEarly Middle Ages,” p. 53. But cf. Thomas Butler, “Yersinia Infections: Centennial of theDiscovery of the Plague Bacillus,” Clinical Infectious Diseases 16 (1994): 660, Fig. 3. Butleris the author of the authoritative Plague and other yersinia infections (New York, 1983).

28 See, for example, A. B. Christie, Infectious Diseases: Epidemiology and Clinical PracticeII (4th ed., Edinburgh and London, 1987), pp. 1038 and 1049.

29 R. H. Cassen, India: Population, Economy, Society (London, 1978), p. 82.30 A. T. A. Learmonth, “Medical Geography in Indo-Pakistan: A study of twenty years’

data for the former British India,” Indian Geographical Journal 33 (1958): 44.31 R. Pollitzer, Plague (Geneva, 1954), pp. 330–331 .32 H. H. King and C. G. Pandit, “A Summary of the Rat-flea Survey of the Madras

Presidency, with a Discussion on the Association of Flea Species with Climate and withPlague,” Indian Journal of Medical Research 19 (1931): 357–392.

33 L. Fabian Hirst, The Conquest of Plague (Oxford, 1953).

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cheopis was thought not to be native to India; in fact, the name cheopis

implies an association with Egypt, and since the publication in 1903of a study by N. C. Rothschild it had been believed that X. cheopis hadprobably originated there.34

When and how had X. cheopis got from Egypt to India? Cassen, itwill be recalled, implied that it had arrived in India only at the timeof the 1896 outbreak. But, very interestingly, King and Pandit thoughtit quite possible that the flea had arrived in India, and begun to para-sitize rats (and maybe other rodents, we are entitled to add), before1896, perhaps well before 1896. Certainly there were Bombay citizensin the late 1890s who, in retrospect, thought that some human casesdisplaying plague-like symptoms had gone unrecognized in the city forat least some months before the existence of plague was officiallydeclared.35 T. S. Weir, the city’s Health Officer at the time of the out-break (and something of a blusterer, it must be admitted), went fur-ther: He claimed in 1898 that “all Hindu and Musalman practitioners”knew the disease and had long been accustomed to treating it.36 Andwe have seen that in 1896 there were some who thought that “Turk-ish Arabia” was the point of origin of the Bombay plague. The pilgrimtraffic between India and Mecca and Medina, and a supposed analogybetween plague and cholera, were probably uppermost in the minds ofthose who made such assertions, but it needs to be remembered thatEgypt, by this stage under de facto British control, was still in reason-ably close touch with the ports of the eastern littoral of the Red Seathat were then part of the Ottoman Empire.

King and Pandit speculated that X.cheopis could have traveled fro mEgypt to India not merely in the months but quite possibly in the yearsbefore plague’s presence in Bombay was officially recognized. It couldhave come, they said, as a result of the “extension of human inter-course and trade (particularly the cotton trade) with Egypt followingthe opening of the Suez Canal in 1869.” They were even prepared tocontemplate an Egyptian origin for visitations of plague—or what hasbeen said to be plague—in India earlier in the nineteenth century,before the opening of the Suez Canal and possibly before the days ofsteamships.37

King and Pandit were daring in their speculations, but not foolish.

34 Robert Traub, “The Fleas of Egypt. Two New Fleas of the Genus Nosopsyllus Jordan,1933,” Proceedings of the Entomological Society of Washington 65 (1963): 96.

35 Snow, Report, p. 1.36 Plague Commission, Minutes of Evidence I, p.44.37 King and Pandit, “Rat-flea Survey,” p. 391.

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T h e re seems no strong reason why—at least occasionally—fleas shouldnot have survived a voyage under sail from the Red Sea area to India.Western India’s trade with the Red Sea ports was of long standing;38 itappears to have undergone something of a decline during much of theeighteenth century but then revived in the last years of that centuryand in the earlier nineteenth century—well before the opening of theC a n a l .3 9 And it seems likely that King and Pandit were right to empha-size the importance of the trade in raw cotton in the spread of plague.For one thing, fleas are apparently particularly attracted by matter thatis white or semi-white.4 0 King and Pandit claimed that a possible out-b reak of plague in Gujarat in 18 15 was linked with Egypt: The BombayP re s i d e n c y, they asserted, “was importing Egyptian cotton at thatt i m e.”4 1 U n f o rt u n a t e l y, t h ey f a i l ed to pro v i de e v i d e n c e on t h is p a rt i c u-lar point. But Egyptian cotton could certainly have been implicated inthe so-called Pali plague which struck Rajasthan in 18 3 6– 3 7. There isevidence of virulent plague in Alexandria in 18 3 4 – 3 5,4 2 and of stro n ge x p o rts of Egyptian long-staple cotton (whose value had only re c e n t l ybeen re c o g n i z e d)4 3 to Bombay in the earlier 18 3 0s .4 4 S i g n i fic a n t l y, thePali plague was said to have begun amongst “Chipahs” who “lived bythe printing of calico brought from the coast.”4 5

Although King and Pandit had nothing to say on the matter, itwould seem to be possible that some, at least, of the pre-nineteenthc e n t u ry episodes on the Indian plains of what has often been said to beplague were also the result of the irregular transfer to Indian rodents of

38 Janet L. Abu-Lughod, Before European Hegemony: The World System, A.D. 1 2 5 0– 1 3 5 0(New York, 1989), pp. 36, 270–272 .

39 Ashin Das Gupta, “India and the Indian Ocean in the Eighteenth Century,” in Indiaand the Indian Ocean 1500–1800, ed. Ashin Das Gupta and M. N. Pearson (Calcutta,1987), pp. 137–140; Third Report from the Select Committee Appointed to Consider the Meansof Improving and Maintaining the Foreign Trade of the Country, PP 1821 (746), vi, esp. evi-dence of J. F. Mitchell (p. 282) and Robert Richards (p. 217).

40 Biraben and Le Goff, “Plague,” p. 53.41 King and Pandit, “Rat-flea Survey,” p. 391.42 James Laidlaw, “Substance of Observations on Oriental Plague, and on Quarantine

as a means of arresting its progress . . . ,” Appendix F to John Bowring, Report on Egypt andCandia, PP 1840 (277), xxi; Daniel Panzac, Quarantine et lazarets: L’Europe et la peste d’Ori-ent (xviie-xxe siècles) (Aix-en-Provence, 1986), p. 20.

43 E. R. J. Owen, Cotton and the Egyptian Economy 1820–1914: A Study in Trade andDevelopment (Oxford, 1969), Ch. II.

44 Bowring, Report on Egypt and Candia, p. 65. Bowring also reported (p. 67) a consid-erable increase in recent years in passenger traffic between Suez and Cosseir [Quseir], inEgypt, and India.

45 Bengal Medical Board, Report on the Malignant Fever called the Pali Plague which hasprevailed in some parts of Rajpootana since the month of July 1836 . . . By James Ranken M.D.(Calcutta, 1838), p. 3.

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X. c h e o p i s, the flea being brought by sea in cargoes directly or indire c t l yemanating from Egypt. In 1631, handloom weavers—working withcotton, it is worth emphasizing—appear to have been very severe l ya ffected by a disease, following famine, which some have thought to bep l a g u e .4 6 T h e re are several other instances of so-called plague in seven-teenth-century India that would bear close investigation. And it maywell be significant that there are few, if any, reports of “plague” in eigh-teenth-century India; during much of that century there was, as wehave seen, a decline in trade between the Red Sea and Persian Gulfareas and the Gujarat coast.

But there is still the problem of what exactly is being referred towhen it is said that parts of India suffered from “plague” in the yearsbefore 1896. Our caution against assuming that plague in India in thelate nineteenth and early twentieth centuries provides a model forother times and other places must surely apply as much to “plague” inIndia in earlier eras as it does to “plague” elsewhere. Until now, mostdiscussion of the problem of the nature of alleged plague in India beforethe nineteenth century has been concerned with whether, in suchre c o rds as we have, rats and buboes are mentioned,4 7 and whether epi-demics are described as ta‘un (said by some to refer specifically toplague) or waba (said to refer to diseases more generally).4 8 Such discus-sion has not been particularly fruitful. But historians of disease in themore distant Indian past—and indeed in the not so distant Indian past—may perhaps take some heart from recent French work in the assess-ment of DNA extracts taken from unerupted teeth in skeletons inmass graves in Provence dating from the sixteenth and eighteenth cen-turies. This has allowed the occurrence of plague in these eras to beconfirmed in a much more exact manner than was previously thecase.49 Will it eventually be feasible to make similar investigations indated graves—they would be Muslim—in, say, Surat? (For that matter,one may add, will it eventually be possible to apply similar techniquesto the fourteenth-century Nestorian graves of the ostensibly plague-

46 M. S. Commissariat, A History of Gujarat . . . , Vol. II., The Mughal Period (Bombay,1957), p. 318.

47 W. H. Moreland, The Agrarian System of Moslem India (1929; reprint, Allahabad,n.d.), p. 145, n. 2 and p. 146, n. 1; M. N. Pearson, “The Thin End of the Wedge: MedicalRelativities as a Paradigm of Early Modern Indian-European Relations,” Modern AsianStudies 29 (1995): 153.

48 Michael W. Dols, The Black Death in the Middle East (Princeton, 1977), Appendix 2.49 Michel Drancourt, Gerard Aboudhram, et al., “Detection of 400-year-old Yersinia

pestis DNA in human dental pulp: An approach to the diagnosis of ancient septicemia,”Proceedings of the National Academy of Science USA, 95 (October 1998): 12637–12640.

1 4 2 journal of world history, spring 2001

ridden found near Lake Issyk-Koul in Kirghizstan, of which some writ-ers50 have made much in attempting to trace the supposed route ofmedieval plague to Europe?)51

A full discussion of the pre–nineteenth-century Indian reports ofplague would have to include some consideration of the possibility thatthe human flea played a more considerable rôle in the transmission ofplague at that time than it did in the India of a century ago. There isstill a school of thought in France that argues not only that the humanflea is important in the spread of plague in such areas as twentieth-cen-t u ry Morocco, Kurdistan, and Iran,52 but also that it was important—even all-important—in Europe at the time of the Black Death.53 Weare entitled to ask whether the same may have been the case in sev-enteenth-century India.

But let us assume for the moment that the appearance of humanplague in India in earlier centuries was at least on occasion related tothe infiltration of rodent-based X. cheopis. Are we then also bound toexplain plague’s periodic disappearance in India’s more distant past atleast to some extent in terms of a diminution of X. cheopis? The storyof Indian plague in the twentieth century may (but, of course, maynot) provide an appropriate analogy.

Cassen, and King and Pandit, believed that, after the nineteenth-century arrival of X.cheopis in India, a “struggle for existence” betweenthe newcomer and X. astia, much longer in India, occurred. By about1920, according to this argument, X. cheopis was the victor in some(but not all) parts of the country. But the victory was shortlived: X.

cheopis began to make way again for “his more congenial predecessors”—and human plague began to decline in India. Yet the matter wasp robably rather more complex than Cassen implied. The evidence thathe produces appears to point to a decline in X.cheopis occurring, in themain, only from about 1960.54 But human plague mortality began to

50 Le Roy Ladurie, “A Concept,” p. 42; McNeill, Plagues and Peoples, pp. 164–165.51 John Norris, “East or West? The Geographic Origin of the Black Death,” Bulletin of

the History of Medicine 51 (1977): 1–24 displayed a healthy skepticism about theories of aCentral Asian origin for the Black Death. But his work belongs, essentially, to an era whenour understanding of DNA was minimal. It may be added that DNA analysis is now beingused to track the history of other diseases besides plague. See Catherine Chauveau, “Oldbones may offer new solutions,” G u a rd i an We e k l y, Le Monde section, 1 0 December 1 9 9 5; andJeffrey K. Taubenberger, Ann H. Reid, et al., “Initial Genetic Characterization of the 1918‘Spanish’ Influenza Virus,” Science 275 (21 March 1997): 1793–1795.

52 M. Baltazard and B. Seydian, “Enquête sur les conditions de la Peste au Moyen-Ori-ent,” Bulletin of the World Health Organization 23 (1960): 157–167.

53 J. C. Beaucournu, “A propos du vecteur de la Peste en Europe Occidentale au coursde la deuxième pandémie,” Bulletin de la Société Française de Parasitologie 1 3 (1 9 95): 233– 2 53.

Catanach: The “Globalization” of Disease? India and the Plague 1 4 3

decline in India some thirty-five to forty years earlier.55 On the face ofit, an intimate connection between the two trends seems somewhatunlikely. The city of Bombay was one of the few places in India wherefleas were closely studied from the 1920s onwards. And in Bombay thestatistics we have for the period 1920–56 appear to show a continuingrise in the percentage distribution of cheopis amongst flea species onrodents. But numbers of fleas per rodent were down in Bombay, andthere was a marked decline in that period in the percentage distribu-tion of the plague-prone black rat in the city, in the face of a distinctrise in the percentage distribution of the bandicoot.56 Similar factorsmay have been important elsewhere in India. But it is worth addingthat in 1960 Baltazard and Bahmanyar reported—with, one suspects,some surprise—“l’absence complète” of X. cheopis (though not, then, acomplete absence of plague) from two districts, Bara Banki and Sah-r a n p u r, in Uttar Pradesh.57 However, X. astia, and another flea, Nosop-

sylla punjabiensis, abounded, and there were some specimens of Xeno-

psylla hussaini, which has many characteristics similar to those of X.

cheopis.

It needs to be noted that the decline of human plague in India after1920 was not a steady decline; a rise in numbers of plague cases duringthe second world war may have been related to the increasing move-ment of food grains from one part of the country to another in the faceof, in particular, famine conditions in Bengal. Still, after the war, thedecline continued, to the extent that, until the 1994 outbreaks, mostIndian authorities on the matter claimed that their last case of humanplague—on the plains, at least—had occurred in 1966.58

* * *

There is certainly room for more debate on the role of fleas in plague.But in our search for reasons for the comings and goings of plague inIndia we must beware of following the flea “trail” too far, at the expense

54 Cassen, India, p. 82 and n. 76.55 Kingsley Davis, The Population of India and Pakistan (Princeton, 1951), p. 46, Fig. 10.56 S. C. Seal, “Epidemiological Studies of Plague in India: 2. The Changing Pattern of

Rodents and Fleas in Calcutta and Other Cities,” Bulletin of the World Health Organization23 (1960), especially p. 296 (Tables 6 and 7) and p. 294 (Table 1).

57 Baltazard and Bahmanyar, “Recherches sur la Peste en Inde,” p. 193.58 Dileep V. Mavalankar, “Indian ‘plague’ epidemic: unanswered questions and key

lessons,” Journal of the Royal Society of Medicine 88 (October 1965): 548, reports seventeendeaths from an outbreak of “primary pneumonic plague” in Himachal Pradesh in 1983. Butthese would be deaths from hill plague, which we have seen as probably unrelated to theplague of the plains.

1 4 4 journal of world history, spring 2001

of other possibilities. Already, in discussing plague’s “decline” in Indiaduring the middle years of the twentieth century, it has become clearthat fleas are not the only non-human variable that must be taken intoaccount. Flea species may “arrive” in India—but they will not surviveunless they can find something congenial to parasitize. We must turnour attention to rodents.

In the 1930s and 1940s, under the leadership of Sir Sahib SinghSokhey at the Haffkine Institute in Bombay, and probably under theinspiration of the work of Ricardo Jorge in the 1920s on “sylvatic”plague, some research was undertaken on Indian rodents of the fieldand forest—as distinct from “commensal” rodents such as the blackrat—and their possible links with plague. The researchers at that timewere not totally united in their conclusions about the matter. Sokheyappears to have believed that, at least in Western India, wild rodentshad no part to play in the plague cycle; two of his re s e a rchers, however,M. Sharif and A. S. Narasimham, were, it seems, not so sure.59 In thelate 1950s Baltazard and Bahmanyar, fresh from their work in Iran andKurdistan, began to research in Northern India—in one of the veryareas where the Plague Research Commission had worked fifty yearsbefore. They concluded that, on the plains of rural Uttar Pradesh, itwas not only human beings and rats that were responsible for thespread of plague from village to village, and for its preservation fromplague “season” to plague “season.” A key rôle was taken by the Indiangerbil, Tatera indica. Baltazard and Bahmanyar argued that, beyond thetowns, underg round gerbil warrens provided the routes by which plaguenormally traveled. The reason for the apparently haphazard nature ofp l a g u e ’s spread in rural Uttar Pradesh now became apparent: these war-rens did not follow straight lines on a map, or roads and tracks made byhuman beings. It was in these warrens, amongst the gerbils, that plaguewas preserved in the heat of the summer and, provided there was noflooding, during the monsoon. At the beginning of the cool season,said Baltazard and Bahmanyar, the gerbils, through their fleas, infected,or reinfected, village rats.6 0 Slightly later French re s e a rchers concludedt h a t, in such u n d e rg ro u nd w a rre n s, “Y. pestis c an s u rv i v e for several y e a r sin the litter of dead animals.”61 In a sense, perhaps, a curious notionfound in India in the 1890s—that plague was “in the soil”—was beingshown to have some basis in fact.

59 Report of the Haffkine Institute for the Years 1940 and 1941 (Government of Bombay,1943), p. 5; cf. pp. 55–60 (the report of Sharif and Narasimham).

60 Baltazard and Bahmanyar, “Recherches sur la Peste en Inde.”61 Guiyoule, Carniel, et al., “Plague Pandemics,” p. 634. The basic work on this mat-

ter seems to have been done in the early 1960s by H. H. Mollaret and others.

Catanach: The “Globalization” of Disease? India and the Plague 1 4 5

It appears that, in India, Baltazard and Bahmanyar studied only therural areas of the plains of Uttar Pradesh. But from the 1960s many ofBaltazard’s conclusions about the role of wild rodents in the diffusionof plague came to be fairly widely accepted as applicable to all plague-prone areas in India. Indeed Baltazard, in a widely circulated summary,in English, of the results of his studies of the world-wide phenomenonof plague, probably seemed to encourage such generalization. He wentso far as to speak of the “somewhat fanciful suggestion that infectedplague fleas were carried from village to village to village in clothing orobjects and produce.” This, he claimed, occurred in India (and also inJava) “only rarely.” 62 It has to be said that this last assertion does notappear to have received general approval from the scientific commu-nity, even in France. It is certainly difficult to explain the speed withwhich plague could, on occasion, move in the rural areas of much ofIndia without giving human beings a significant role. Nevertheless, itis most important that the historian, for whom people are normallythe prime concern, should not ignore Baltazard’s warnings about thedangers of “l’anthropocentrisme” in plague matters.63

Baltazard had, of course, amongst other things, heavily underlinedthe fact that plague was essentially a disease of rodents; its transmissionto human beings, when it occurred, was incidental, not a vital part ofits history in Nature. For that re a s o n—and perhaps also because he wasstill something of a product of the essential optimism of the era of the“ l a b o r a t o ry re v o l u t i o n ” — B a l t a z a rd b e l i e v ed t h at h u m an b e i n gs in I n d i acould do much to control their destiny so far as plague was concern e d.Furthermore, although Baltazard believed that there were pockets oflong-lasting plague infection amongst wild rodents in the rural areasof North India, he also believed that they were not absolutely perma-nent. Baltazard asserted that, unlike the “reservoirs” of plague amongstwild rodents in, for example, Kurdistan, these underground Indianplague “foci” had come into being only since the end of the nineteenthcentury. (Like almost everybody else in his day he accepted the theoryof plague’s sudden arrival in India, by steamship, in 18 9 6.) Because theyhad not had long to establish themselves the underground plague fociin India were, Baltazard thought, very limited in extent. Baltazard rec-ommended a campaign aimed at the eradication of these foci.6 4 He maywell have underestimated the size of such a task. Be that as it may:

62 Baltazard, “Epidemiology of Plague,” pp. 421–422.63 M. Baltazard, “Déclin et Destin d’une Maladie infectieuse: la Peste,” Bulletin of the

World Health Organization 23 (1960): 255.64 Baltazard and Bahmanyar, “Recherches sur la Peste en Inde,” p. 211, and (particu-

larly) the English “Summary” of this article on p. 214.

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What seems to have happened in practice in India as a whole from themid-1960s was that foci of sylvatic plague were identified and thensimply kept under “surveillance.” With the apparent “disappearance”of human plague from the Indian plains after 1966 little more mayhave seemed necessary.

* * *

But the years since the mid-1960s have seen many developments inthe study of plague, both human and sylvatic, and both in India andelsew h e re—developments that are very relevant to our concerns ashistorians. There has been, for example, a good deal of work, by theZoological Survey of India and others, on the habits of wild and “peri-commensal” rodents. We now know just what a large diff e rence theadvent of irrigation in hitherto dry areas can make to the size of wildrodent populations.6 5 We surely now have something of an explanationfor the widespread human plague in the newly irrigated areas of thePunjab in the first decade of this century. It is an explanation in which,it must be admitted, human beings and their technology are primary.But the same point cannot easily be made about recent work on theways in which earthquakes may be connected with human plague.E a rthquakes can break up the established warrens of wild rodents, andsend some of those cre a t u res scurrying in the direction of human settle-m e n ts—p a rt i c u l a r l y, perhaps, temporarily deserted settlements, whereu n d e rg round stores of grain may be broken open by the quakes.6 6

By the early 1990s the government of Maharashtra, in WesternIndia, had largely abandoned, as a needless expense, its sylvatic plaguesurveillance activities. Nevertheless, there were warnings, after theMaharashtra earthquake of September 1993, of the possibility of anoutbreak of human plague.67 Not everyone was totally surprised by theadvent of what was said to be bubonic plague in the Beed area ofMaharashtra—very near, so it would seem, one of the foci of sylvaticplague 68 —in August 1994.

It must also be said that recent years have seen a somewhat more

65 Anamitra Choudhury, “Tiny Terrors,” Down to Earth: science and environment fort-nightly (New Delhi), 30 November 1995, pp. 34–35.

66 “Unheeded Signposts,” editorial, Economic and Political Weekly (Bombay), 24 Sep-tember 1994; Elisabeth Carniel, “Situation mondiale de la peste,” Médicine et Maladiesinfectieuses 25 (1995, Spécial): 678. More work needs to be done on possible connectionsbetween earthquakes and plague in China, as well as, of course, in the Himalayan foothillsof India.

67 G. Nandan, “Troops battle to contain India’s outbreak of plague,” British MedicalJournal 309 (1 October 1994): 827; also, “Unheeded Signposts” (see above, n. 66).

68 M. Sharif, “Spread of Plague in the Southern and Central Divisions of BombayProvince and Plague Endemic Centres in the Indo-Pakistan Subcontinent,” Bulletin of the

Catanach: The “Globalization” of Disease? India and the Plague 1 4 7

precise understanding of pneumonic, as distinct from bubonic, plague—an understanding that may have a bearing on our conclusions aboutother “plague” episodes in India besides the supposed pneumonic out-break at Surat in 1994. Increasingly, plague in medieval Europe is seenas likely to have been pneumonic, or at least predominantly pneu-monic, rather than bubonic.6 9 For one thing, there is a “scarcity of rats”(and, by implication, their fleas) in the re c o rds. Rats and fleas are nor-mally associated with bubonic cases, although it has been asserted that“plague” buboes are not invariably the result of flea bites.7 0 We mightv e n t u re to speculate that Europe will ultimately provide us with moreof a “norm” for plague in the overall span of human history than latenineteenth and early twentieth-century India. We should probably notbe surprised if some of the more mysterious “plague” episodes in India’sm o re d i s t a nt p a s t — f or e x a m p l e, s e v e n t e e n th- c e n t u ry e p i s odes in w h i c ht h e re m ay be f e w, if any, re p o rts of buboes— p ro ve to b e, on closer inves-tigation, o u t b reaks of some form of pneumonic plague.

Nor should we be enormously surprised that in 1994 there were—at first, at least—said to be no cases of bubonic plague at Surat, eitherpreceding or contemporaneous with the pneumonic attacks.71 TheSurat outbreak may have had little or no connection with the bubonicoutbreak at Beed—over three hundred kilometers away—a few weeksbefore.72 There had been heavy monsoon floods in and around Surat:people had come into contact, in various ways, with dead or dying ani-mals that could well have been plague-infected. Authorities from theCenters for Disease Control in the United States now tell us plainlythat “persons can . . . acquire plague by handling infected animals orby exposure to respiratory droplets from . . . animals with pneumonicplague.”73 Here, on the face of it, is a sufficient explanation for the

World Health Organization 4 (1951): 101; M. V. Sant, Y. S. Nimbkar, and D. M. Renapurkar,“Is Plague Lurking in Maharashtra? A Survey in Bhir District,” Indian Journal of Medical Sci-ences 26 (1972): 480 –484.

69 The point was made forcefully by Christopher Morris in his well-known review arti-cle on J. F. D. Shrewsbury, A History of Plague in the British Isles in the Historical Journal 14(1971), especially pp. 207–209. See also Gunnar Karlsson, “Plague without rats: The caseof fifteenth-century Iceland,” Journal of Medieval History 22 (1996): 263–284.

70 David E. Davis, “The Scarcity of Rats and the Black Death: An Ecological History,”Journal of Interdisciplinary History 16 (1986): 461. But Christopher Wills, Plagues: Their Ori-gin, History and Future (London, 1996), p. 13, states a very commonly held view when hesays that bubonic plague “can only be spread by fleas.”

71 The claim that there had been forty-one cases of bubonic plague in Surat in 1994came very late in the day: Statesman (Delhi), 14 March 1995.

72 But see Robert D. Perry and Jacqueline D. Fetherston, “Yersinia pestis—EtiologicAgent of Plague,” Clinical Microbiology Reviews 10 (1997): 56.

73 Grant L. Campbell and James M. Hughes, “Plague in India: A N ew Wa rning from anOld Nemesis,” Annals of Internal Medicine 122 (1995): 151.

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Surat episode of 1994. Here, too, it might be added, is—conceivably—a hitherto unnoticed explanation for at least some of the plague inBombay in 1896. It will be remembered that such pneumonic cases asthere were in 1896 tended to come at the beginning of the epidemic.Furthermore, the monsoon rains in Bombay had been unusually heavyin that year, and flooding was even more prevalent than usual. Trafficto Bombay Island was disrupted for five days.74 It all sounds, in fact,remarkably like Surat in 1994. Of course, if those floods in Bombay in1896 brought to the city animals that were already plague-infected,another possible argument against plague “arriving” in India in thatyear, from China or with a flea from Egypt, would become apparent.That—particularly in view of the possibility of pneumonic plaguee p i s odes earlier i nI n d i a ’s history—p e rh a ps n e ed n ot c o n c e rn us unduly.

What is required, of course, is a readiness to admit the possibilitythat, even if in the final analysis the “foci” of sylvatic plague in theplains of India as a whole are “temporary,” as Baltazard believed wasthe case, some of these foci, at least in Western India, could have beenalready present in 1896. Such an admission would not necessarilyinvolve a major paradigm shift.

It will be remembered that Baltazard appears to have worked inIndia only on the plains of Uttar Pradesh; Western India, as we haveseen, had long been more open to influences coming from afar by sea.Certainly, an admission that plague could have established itselfamongst wild rodents in We s t e rn India before 18 9 6 would allow one tosay that those who sought some sort of local origin for Bombay plaguein 1896 were not totally misguided.

* * *

Such an admission would also allow us to consider whether the epi-demic of 18 9 6 and the following years could have had its origin, at leastin part, in changes taking place—within India, around 1896—in theplague pathogen itself. It is to the possible historical implications ofrecent research on the genetic structure of the bacterium Y. pestis thatwe now, finally, turn. We are turning, it is worth reminding ourselves,to the most fundamental of all the “causes” of the disease, in the sensethat without Y. pestis there would be no plague.

Yersinia pestis is one of a group of closely related bacteria, the Yersi-

74 L. W. Michael, comp., The History of the Municipal Corporation of the City of Bombay(Bombay, 1902), p. 189; Bombay Gazette, 24 and 31 July, 1 August 1896.

Catanach: The “Globalization” of Disease? India and the Plague 1 4 9

niae. It is, says Christopher Wills, an “unnervingly close” relative of theless “virulent” Yersinia pseudotuberculosis75—to the extent that somehave thought that Y. pestis might at times in the past have mutated intoY. pseudotuberculosis, thus bringing some plague epidemics to a close.(In fact, in the earlier 1980s—“unnervingly” again—the reverse pro-cess seemed to Stephen R. Ell to be “at least as likely.”)76 In 1988 sci-entists at Umeå in Sweden succeeded in producing two small geneticmutations in Y. p s e u d o t u b e rculosis; the bacteria became a hundred timesm o re virulent. This led the team to speculate that similar “single point”mutations occurring “naturally” in Y. pestis might have been the re a s o nfor epidemics—in the sense of sudden rises of viru l e n c e—of plagueamongst humans in the past; similar mutations might also explain thedecline of epidemics.7 7 In such a scheme of things, it should hardly benecessary to observe, humans played only a passive rôle.

A commentator in N a t u re immediately pointed out that “mutationsalone cannot drive epidemics.” One had to take “hosts” (of a numberof varieties, one might add) into account, and in particular considerwhether the extended and recurring nature of many “epidemics” wasat least to some extent the result of pathogens being comparatively“nice”, rather than particularly “nasty”, to their hosts. It was not in theinterest of the parasite to kill off all hosts.78 Such points were wellmade. Then, in a paper published in 1997, it was shown that theSwedish research of the late 1980s was seriously at fault, in that themutants used in that research were not “isogenic to the parental wild-strain”; new “constructs” of the relevant mutants were no more viru-lent than the Y. pseudotuberculosis that occurs at present under naturalconditions.79

Yet it cannot be said that this latest work on mutation in Y. pseudo-

tuberculosis has brought tumbling to the ground all the daring hypoth-eses of 1988 about the nature and effects of mutation in Y. pestis. Some

75 Wills, Plagues, p. 73 (but Y. pestis is assuredly not the “same thing” as Y. pseudotuber-culosis—as Robert R. Brubaker, “Molecular Biology of the Dread Black Death,” ASM News[American Society for Microbiology] 50 [1984]: 244, emphasizes).

76 Stephen R. Ell, “Immunity as a Factor in the Epidemiology of Medieval Plague,”Reviews of Infectious Diseases 6 (1984): 870.

77 Roland Rosqvist, Mikael Skurnik, and Hans Wolf-Watz, “Increased virulence ofYersinia pseudotuberculosis by two independent mutations,” Nature 334 (14 August 1988):522–525.

78 Richard E. Lenski, “Evolution of Plague Virulence,” ibid., pp. 473–474. Baltazardhad made a similar point in 1960: “Epidemiology of Plague,” p. 419.

79 Yiping W. Han and Virginia L. Miller, “Reevaluation of the Virulence Phenotype ofthe inv yadA Double Mutants of Yersinia pseudotuberculosis,” Infection and Immunity 65(1997): 327–330.

1 5 0 journal of world history, spring 2001

of the conclusions that have emerged about the Surat epidemic of 1 9 9 4provide quite powerful reasons for the historian to continue to attendcarefully to the matter of mutation. There were at first great problemsabout contamination of bacteriological samples taken at Surat. Buteventually—after much work in India, the United States, Russia, and,especially, in the Plague Reference Laboratory headed by ElisabethCarniel at the Institut Pasteur in Paris—it was announced that the1994 Surat outbreak was definitely one of plague. The Surat strain,however, was found to be “new,” in the sense that it had not previouslybeen identified, and what was more, it possessed a “ribotype” (rRNAgene pro file) hitherto unknown. In other words, the 1 9 9 4 Surat versionof Y. pestis did not match in all of its characteristics the Y. pestis a s s o c i-ated with the plague commonly asserted to have appeared in Indiaalmost a century before; nor did it match completely the characteris-tics of the supposed mod e rn remnants of either the Plague of Justinianor the Black Death. This is not to say that the Surat strain was n e c e s-

sarily a recent mutation, but a mutation it certainly seemed to be, anda significant one at that.8 0 M o re evidence about the possibilities ofmutation came in 1 9 9 7 f rom work, largely French, in Madagascar.T h e re, no fewer than three “new” Y.pestis ribotypes have recently beend i s c o v e re d. Furt h e rm o re, a Madagascar strain of Y. pestis first found in1 9 9 5 is causing considerable concern because, unlike all other knownstrains of Y. p e s t i s, it is resistant to common antibiotics. Again, thisstrain has not necessarily evolved re c e n t l y, but, given that the watchon plague in Madagascar has been fairly close since 1 9 2 6, it seemslikely that it has done so.8 1

A very interesting commentary on the possibilities of mutation inY. pestis has recently been provided by a French team in which, again,Elisabeth Carniel has played a prominent part. It would appear that a

80 “Report of the Technical Advisory Committee on Plague: Summary”, reprinted asAppendix D of Ghanshyam Shah, Public Health and Urban Development: The Plague in Surat(New Delhi, 1 9 9 7); V.Ramalingaswamy et al., “Plague in India,” N a t u re Medicine 1 ( D e c e m-ber 1995): 1237–1239, is a slightly expanded version of this summary. Annie Guiyoule,Elisabeth Carniel, and others, shortly before the Surat outbreak, had classified on the basisof DNA probes the makeup of seventy strains from which isolates, from various times (from1908) and places, were available. (See n. 21 above.) But there are many Y. pestis strains stillto be classified in this way.

81 Annie Guiyoule, Elisabeth Carniel, et al., “Recent Emergence of New Variants ofYersinia pestis in Madagascar,” Journal of Clinical Microbiology 35 (1997): 2826–2833; MarcGalimand, Annie Guiyoule, Elisabeth Carniel, et al., “Multidrug Resistance in Yersiniapestis Mediated by a Transferable Plasmid,” New England Journal of Medicine 337 (Septem-ber 1997): 677–680; also David T. Dennis and James M. Hughes, “Multidrug Resistance inPlague,” ibid., pp. 702–704.

Catanach: The “Globalization” of Disease? India and the Plague 1 5 1

strain of Y. pestis found in 1963 in Nhatrang, Vietnam, is of the biovarOrientalis. Its ribotype is the same as a ribotype today found elsewhereonly in Kenya. But, most surprisingly, in spite of this similarity of ribo-type, the biovar in Kenya is not Orientalis but Antiqua. The Frenchresearchers offer the following comment on this situation. “The exis-tence of strains of ribotype G in Kenya and Nhatrang may indicate acommon origin; however, the fact that the strains from these two coun-tries do not have the same biovar may also indicate that a similar muta-tion occurred independently in the rDNAs of these two groups of bac-teria.”82 The possibility of similar bacteriological developments in Y.

pestis occurring “independently,” in two places very distant from eachother, is surely here acknowledged. The implications of such a possi-bility for the history of plague—including, even, the supposed HongKong–Bombay link in 1896—could be considerable. At the least, thepossibility of independent mutation of similar strains would surelymean that the first question to be asked about any past outbreak ofplague would not necessarily have to be “Where did the disease comefrom?” Nor, perhaps, would the next question always have to be“Where did it spread to?”

Having said this it must be added that the old questions of geo-graphical origin and of potential and actual spread must never be for-gotten. People in the past believed these questions to be important;that fact alone makes them significant for the historian. And certainly,with the evidence before us of such recent developments as the anti-b i o t i c - resistant Madagascar strain, both historians and scientists wouldbe foolish indeed not to continue to ask such questions. But we mustdo so in a broader context than has often been the case in the morerecent past. In particular we must not forget about the possibilities ofmutation.

So far as mutation is concerned we may probably take some com-fort from the likelihood that many strains of Y. p e s t is—including newstrains—remain amongst animals, and do not make the jump tohuman beings.8 3 And we may certainly take some comfort from the factthat Indian experience, past and present, shows that some strains pro-duce only quite minor reactions in humans. We cannot at present be

82 Guiyoule, Carniel, et al., “Plague Pandemics,” p. 640. This is not to imply that theseauthors would necessarily agree with the conclusions that are drawn here.

83 Cf. Wills, Plagues, pp. 84–85. John Hatcher, a prominent British authority on medi-eval plague, is well aware of this probability. He is quoted by Gavin Weightman, “Maybethe black rat didn’t do it,” The Independent on Sunday (London), 9 October 1994, as sayingthat a human plague episode on the scale of the Black Death “may only happen once every10,000 years.”

1 5 2 journal of world history, spring 2001

entirely sure that the disease which struck Beed in Maharashtra in1994 really was plague. Problems of identification were even greater atBeed than they were in Surat. All we can say is that a WHO team con-cluded that it was very likely that the Beed disease was plague.84 But ifit was plague it must have been of a very benign variety. Not a singleperson died in Beed as a result of the 1994 outbreak; this is mostunusual in modern plague, and it must be said that it is hardly to beexpected in present-day India, even given the fact that supplies oftetracycline were rushed to the area. (The outbreak at Surat, by con-trast, killed at least fifty people.) An almost forgotten term, Pestis

minor, was revived in an effort to describe the Beed disease.85 Quitepossibly the same term could also be applied to some episodes in India’smore distant past where surviving records show that some, but not all,of the “classical” plague symptoms were present.

* * *

The picture we have, increasingly, then, is one of a disease which hasmany faces;86 plague does not possess a single, immutable identity. (Atthe same time it is not simply what we care to call plague: there is notmuch to be said for nominalism in medical matters.)87 Rats and theirfleas undoubtedly have had a large part—though not an unchangingp a rt—to play in the spread of plague in mod e rn India, but, so too, havewild rodents. The possibilities that wild rodents, and also the h u m a nflea, had significant roles in the spread of human plague in India in ear-lier centuries cannot be dismissed. How plague actually originated inIndia in the late nineteenth century, and indeed in earlier centuries,remains something of a mystery. It may well have come by sea, fromother parts of the world—sometimes, perhaps, with an Egyptian fleain bales of raw cotton.

The generally accepted theory of a Hong Kong origin for the plaguewhich appeared in Bombay in 1896 remains a reasonably viable one.B u t we m u s t at least consider the possibility that human plague in 18 9 6,in 1 9 9 4, and at other times, originated within India rather than beyond

84 “Plague in India: World Health Organization International Plague InvestigativeTeam Report, 9 December 1994” (typescript), reprinted as Appendix C of Shah, PublicHealth and Urban Development.

85 Mavalankar, “Indian ‘plague’ epidemic,” p. 548; and Carniel, “Situation mondiale,”p. 675 (cf. evidence of H. P. Dimmock, Plague Commission, Minutes of Evidence III, p. 120).

86 But it needs to be noted that Guiyoule, Carniel, et al., “Plague Pandemics,” p. 634,find more “homogeneity” in Y. pestis than in many other bacteria.

87 Cf. Brubaker, “Molecular Biology,” p. 244.

Catanach: The “Globalization” of Disease? India and the Plague 1 5 3

its shores, ultimately as a result of mutations in Y. pestis and in otherclosely related organisms. “I have for long entertained the belief thatthe great majority of epidemics arise where they occur,” wrote GeorgeWaters in Bombay in 1896.88 This may seem, at first sight, to be tau-tological; to us today Waters may seem to be one of the dafter mem-bers of the Indian Medical Service. (That, indeed, was the opinion ofsome in the 1890s.)89 Yet the miasmatically inclined Waters perhapshad a point: Some plague epidemics may indeed “arise where theyoccur.” There may be no need to look for an origin elsewhere. Theidea of “globalization” (a “globalization” in which human beings playa dominant part) may not always be of great relevance when it comesto plague.

An explanation of plague’s origin that gives a significant role tomutation, like an explanation of plague’s spread that gives a large roleto wild rodents, may be unsatisfying to anthropocentric historians, andto anthropocentric contemporary re p resentatives of the essentially tri-umphalist age of the “l a b o r a t o ry revolution” in medicine. But, as inother matters, it is perhaps time that, without an undue tolling of bellsof alarm, our limitations as human beings were more openly re c o g n i z e d.

88 Waters, “The Bombay Plague,” p. 430.89 J. deC. Atkins, Secre t a ry, Government of Bombay, General Department, to Govern-

ment of India, No. 1411 of 5 September 1897, India Home Medical Proceedings, Novem-ber 1897, 89, National Archives of India, New Delhi.