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Hoe pokke die Asteke verwoes het - en 500 jaar gelede Spanje gehelp het om 'n Amerikaanse beskawing te verower
Richard Gunderman werk nie vir, raadpleeg, besit aandele in of ontvang befondsing van enige onderneming of organisasie wat baat by hierdie artikel nie, en het geen relevante verbintenisse bekend gemaak buiten hul akademiese aanstelling nie.
Vennote
Indiana University bied finansiering as lid van The Conversation US.
Die Conversation UK ontvang befondsing van hierdie organisasies
Onlangse uitbrake in die VSA het die aandag gevestig op die gevare van masels. Die Demokratiese Republiek van die Kongo beveg 'n dodelike uitbraak van Ebola wat honderde mense doodgemaak het.
Epidemies is natuurlik niks nuuts nie. En sommige wydverspreide aansteeklike siektes het die verloop van die menslike geskiedenis ingrypend verander.
Vyfhonderd jaar gelede, in Februarie 1519, vaar die Spanjaard Hernán Cortés uit Kuba om die Aztec -beskawing in die Mexikaanse binneland te verken en te koloniseer. Binne twee jaar was die Azteke heerser Montezuma dood, die hoofstad Tenochtitlan is gevange geneem en Cortés het die Asteke -ryk vir Spanje geëis. Spaanse wapens en taktiek het 'n rol gespeel, maar die grootste deel van die vernietiging is veroorsaak deur epidemies van Europese siektes.
Vroeë beheerpogings
Pokke was 'n vreeslike siekte. Gemiddeld sterf 3 uit elke 10 mense wat dit gekry het. Mense wat oorleef het, het gewoonlik letsels gehad, wat soms ernstig was.
Een van die eerste metodes om pokke te bestry, was variolation, 'n proses vernoem na die virus wat pokke (variola -virus) veroorsaak. Tydens variolasie is mense wat nog nooit pokke gehad het nie blootgestel aan materiaal van pokkies (pustels) deur die materiaal in hul arm te krap of deur die neus in te asem. Na afwyking ontwikkel mense gewoonlik die simptome wat verband hou met pokke, soos koors en uitslag. Minder mense sterf egter aan variolasie as as hulle pokke natuurlik opgedoen het.
Die basis vir inenting het in 1796 begin toe die Engelse dokter Edward Jenner opgemerk het dat melkmeisies wat koeipokke gekry het, teen pokke beskerm is. Jenner weet ook van variolasie en vermoed dat blootstelling aan koeipokke gebruik kan word om teen pokke te beskerm. Om sy teorie te toets, het dr. Jenner materiaal geneem uit 'n koeipokkie wat seer was op die melkmeisie Sarah Nelmes en het dit in die arm van James Phipps, die 9-jarige seun van Jenner & rsquos tuinier, ingeënt. Maande later het Jenner Phipps verskeie kere aan variola -virus blootgestel, maar Phipps het nooit pokke ontwikkel nie. Meer eksperimente het gevolg, en in 1801 het Jenner sy verhandeling gepubliseer oor die oorsprong van die entstof. In hierdie werk het hy sy ontdekkings opgesom en hoop uitgespreek dat die pokkel, die vreeslikste plaag van die menslike spesie, uitgewis moet word wees die finale resultaat van hierdie praktyk. & rdquo
Inenting word algemeen aanvaar en het geleidelik die praktyk van variolasie vervang. Op 'n stadium in die 1800's het die virus wat gebruik word om die pokke -entstof te laat verander, verander van koeppokke na vaccinia -virus.
Spore van pokke op die kop gevind op die kop van die 3000-jarige mummie van die farao Ramses V. Foto met vergunning van die Wêreldgesondheidsorganisasie (WGO)
Edward Jenner (1749 en ndash1823). Foto met vergunning van die National Library of Medicine.
Inentingsoorwinning
Die menslike stryd teen pokke dateer ongeveer 2 000 jaar terug. In Asië het 'n tegniek, bekend as variolation, doelbewus 'n persoon besmet deur gedroogde pokke op hul neus op te blaas. Diegene wat hierdie behandeling ontvang het, het 'n ligte vorm van die siekte opgedoen en 'n lewenslange immuniteit ontwikkel.
'N Belangrike deurbraak kom in 1796 toe 'n eksperiment deur die Engelse dokter Edward Jenner toon dat inenting met nou verwante koeipokke teen pokke kan beskerm. Die ontdekking van Jenner het die weg gebaan vir latere inentingsprogramme - veral belangrik, aangesien daar geen effektiewe behandeling vir pokke is nie.
In 1967, 'n jaar toe ongeveer 10 miljoen tot 15 miljoen mense pokke opgedoen het, het die Wêreldgesondheidsorganisasie 'n wêreldwye uitroeiingsveldtog op grond van inenting geloods. Geleidelik word die siekte teruggestoot na die Horing van Afrika, en die laaste bekende natuurlike geval het in 1977 in Somalië voorgekom.
Het vroeë Europese ontdekkingsreisigers werklik inheemse Amerikaners pokke besmet?
As die vraag gevra word: Het die vroeë Europese ontdekkingsreisigers werklik inheemse Amerikaners pokke besmet?, Sou die meeste mense die vraag as belaglik vind. Dit mag egter nie so vergesog wees nie. Of dit nou werklik gebeur het of nie, is oop vir debat, maar daar is voldoende bewyse om aan te toon dat die presiese daad as 'n oorlogsinstrument teen inheemse Amerikaanse Indiane beskou is.
Geskiedenis van pokke
Die eerste bekende geval van die pokke het in 1507 op die eiland Hispaniola plaasgevind. Hierdie eiland staan vandag bekend as Haïti en die Dominikaanse Republiek. Baie meen dit was die Spaanse ontdekkingsreisiger Herman Cortes en 600 soldate wat die siekte gebruik het om miljoene Asteke in 1520 te verslaan. Pokke het heel waarskynlik na Amerika gekom deur die pelgrims wat in Massachusetts geland het. Teen die middel van die 18de eeu het pokke oor die hele land duidelik versprei. Aangesien die siekte vir lang tye van lap of stof kan leef, het dit so vinnig versprei dat dit 30% van alle Indiërs wat besmet geraak het, uitgewis het. Pokke het moontlik ook 'n rol gespeel in die uitwissing van die Taino van die Bahamas en die Groter Antille.
Die Pokke Plan
In 1763 was die Britse magte tydens die Rebellie van Pontiac in 'n geveg met die Ottawa -stam betrokke. Volgens dokumente wat ontdek is deur Peter d ’Errico, professor in regstudies aan die Universiteit van Massachusetts in Amherst, het Lord Jeffrey Amherst, bevelvoerder van Britse magte in Noord -Amerika, na bewering 'n brief aan kolonel Henry Bouquet gestuur. In hierdie brief het hy blykbaar die moontlikheid bespreek om die Indiane met pokke in te ent deur die gebruik van komberse. Hierdie werklike brief is ooit ontdek, maar ander korrespondensie tussen Amherst en Bouquet dui beslis op die bestaan van so 'n brief.
Is die plan uitgevoer?
Die antwoord op hierdie vraag is dat niemand regtig weet nie. Wat bekend is, is dat dit moontlik was, aangesien daar komberse by Fort Pitt beskikbaar was waar die siekte onlangs ontdek is. Die ander faktor wat so 'n mal plan haalbaar was, was die siening van Amherst oor die inheemse Amerikaanse Indiër as iets op die vlak van 'n hond. Hy het aangedui dat hy dink dat dit 'n vermorsing van goeie mense is om na hierdie diere (die Ottawa) te gaan, en hy het maniere gesoek om dit uit te skakel sonder om die lewens van sy mans in gevaar te stel. Hy het selfs verwys na dieselfde metodes wat die Spaanse gebruik het om die Asteke te verslaan.
So, wat is die antwoord op die vraag. Het vroeë Europese ontdekkingsreisigers werklik komberse wat met pokke besmet is, inheemse Amerikaners gegee? Die waarheid is onbekend, maar hulle is omstandigheidsgetuienis genoeg om 'n redelike bewering te maak. Die Britse offisier het gepraat oor die moontlikheid om dit werklik te doen, komberse was beskikbaar, die bedrieglike ingesteldheid was in plek en baie Indiërs het aan die siekte gesterf. Dit is so 'n diaboliese idee dat die meeste mense dit onbegryplik vind. Maar die feit bly staan, dit was oorlogstye en die Britse soldate was in oorlog.
Weergawe een: 1992
Churchill het die vroegste bekende herhaling van sy pokkekombersfabel in 1992 gepubliseer, as een hoofstuk van 'n boek onder redaksie van M. Annette Jaimes, wat destyds Churchill se vrou was. Die outeurskap van die hoofstuk is egter na "Lenore A. Stiffarm with Phil Lane, Jr." Dit lyk asof hulle regte mense is. In 2006, as deel van Churchill se verweer teen aanklagte van plagiaat, beweer hy dat hy hierdie hoofstuk spookgeskryf het (Wesson et al, 2006, p. 40, vn. 78). Die ondersoekkomitee van die Universiteit van Colorado oor wangedrag in navorsing het Churchill se eis oor spookskryf ter waarde aanvaar. Die hoofstuk bevat inderdaad die stilistiese kenmerke van Churchill en herhaal die vervaardigde besonderhede wat Churchill nog ses keer onder sy eie naam sou herpubliseer.
Deur sodoende 'n aanklag van plagiaat te ontduik, het Churchill hom egter kwesbaar gemaak vir nuwe aanklagte van vervaardiging en vervalsing met betrekking tot sy pokke -kombersvertelling. Die hoofstuk "Stiffarm and Lane" (1992) beweer dat:
Die verspreiding van komberse wat besmet is deur pokke deur die Amerikaanse weermag aan Mandans by Fort Clark, aan die Missouri-rivier in die huidige Suid-Dakota, was beslis die oorsaak van die pandemie van 1836-1840. (bl. 32)
Die eindnota van "Stiffarm en Lane" lui:
Die komberse is van 'n hospitaal van die Amerikaanse weermag in St. Hulle is op 19 Junie 1837 deur weermagpersoneel versprei. Sien Chardon, Francis A., Journal at Fort Clark, 1834-39, State Historical Society of South Dakota, Pierre, 1932. (p. 50, vn. 55)
Veilig weggesteek agter 'n neplyn, begin Churchill 'n ad hominem -aanval op Russell Thornton, die skrywer wie se sterfteskattings Churchill op staatmaak vir sy pokkekombers. In die gedaante van 'Stiffarm en Lane' noem Churchill Thornton '' 'n ietwat deurmekaar Cherokee -demograaf. ' geleerdes [.] "(p. 27).
Siekte was nog nooit net 'n siekte vir inheemse Amerikaners nie
Die kwesbaarheid van inheemse gemeenskappe vir epidemies is nie 'n historiese ongeluk nie, maar 'n direkte gevolg van onderdrukkende beleid en voortgesette kolonialisme.
Oor die skrywer: Jeffrey Ostler is die Beekman -professor in die geskiedenis van Noordwes en die Stille Oseaan aan die Universiteit van Oregon. Hy is die skrywer van Oorlewende volksmoord: inheemse nasies en die Verenigde State van die Amerikaanse revolusie tot bloedende Kansas.
Namate die dodetal van COVID-19 toeneem, loop mense van kleur duidelik 'n groter risiko as ander. Onder die kwesbaarstes is inheemse Amerikaners. Om te verstaan hoe erg die COVID-19-situasie vir hierdie gemeenskappe word, oorweeg die situasie wat ontvou vir die Navajo-nasie, 'n bevolking met tuislande in Arizona, New Mexico en Utah. Op 23 April is 1,360 infeksies en 52 sterftes aangemeld onder die 170,000 mense van die Navajo -reservaat, 'n sterftesyfer van 30 per 100,000. Slegs ses state het 'n hoër tol per capita.
Die verspreiding van COVID-19 herinner aan vorige siekte-uitbrake wat inheemse Amerikaanse gemeenskappe geteister het. Baie van die uitbrake het katastrofiese lewensverliese tot gevolg gehad, veel groter as selfs die ergste scenario's vir COVID-19. Selfs die grieppandemie van 1918-1919, waarin na raming 650 000 Amerikaners gesterf het (0,6 persent van die 1920 -bevolking van 106 miljoen), word ligter in vergelyking met die verliese wat inheemse Amerikaners aan siektes gely het.
Tot onlangs het die geskiedenis van siektes en inheemse Amerikaners die klem gelê op "maagdelike epidemies." Volgens hierdie teorie, gewild onder Jared Diamond's Gewere, kieme en staalToe Europeërs in die Westelike Halfrond aankom, het hulle siektes (veral masels en pokke) gebring wat inheemse mense nog nooit beleef het nie. Omdat hulle geen immuniteit teen hierdie siektes het nie, so volgens die teorie, het die gevolglike epidemies die lewe van 70 persent of meer van die inheemse bevolking in die hele Amerikas geneem.
Nuwe navorsing bied egter 'n baie meer ingewikkelde beeld van siektes in die Amerikaanse Indiese geskiedenis. Hierdie navorsing toon dat die epidemies van maagdelike grond nie so algemeen was as wat voorheen geglo is nie en verskuif die fokus na hoe siektes in die dekades en eeue herhaaldelik die inheemse gemeenskappe aangeval het daarna Europeërs het eers aangekom. Na-kontak siektes was nie so verlammend nie omdat inheemse mense nie immuniteit gehad het nie, maar omdat die toestande wat deur die Europese en Amerikaanse kolonialisme geskep is, inheemse gemeenskappe kwesbaar gemaak het. Die hipotese van maagdelike grond-epidemie was waardevol in die stryd teen vroeëre teorieë wat die agteruitgang van die inheemse Amerikaanse bevolking aan rasse-minderwaardigheid toegeskryf het, maar die unieke klem op biologiese verskil impliseer dat die ineenstorting van die bevolking niks anders as historiese ongelukke was nie. Deur die belangrikheid van sosiale toestande wat deur menslike besluite en optrede geskep word, te beklemtoon, bied die nuwe beurs 'n veel meer ontstellende beeld. Dit help ons ook om die probleme van inheemse gemeenskappe vandag te verstaan terwyl hulle die nuwe koronavirus bestry.
Maagdgrond-epidemies het ongetwyfeld voorgekom. In 1633 het 'n pokke -epidemie byvoorbeeld inheemse gemeenskappe in New England getref, wat die bevolking van Mohegan en Pequot verminder het van 'n totaal van 16,000 tot slegs 3,000. Die epidemie het na die Haudenosaunee in New York versprei, maar nie verder wes as dit nie. Pokke het gemeenskappe in die Ohio -vallei en Great Lakes eers in 1756–57 getref, 'n eeu of meer na die eerste kontak met Europeërs. Toe dit gebeur, was dit omdat inheemse vegters wat tydens die sewejarige oorlog vir die Franse teen die Britte geveg is, die virus in die ooste opgedoen het en hul gemeenskappe besmet het toe hulle teruggekeer het huis toe. Gebrek aan immuniteit was belangrik, maar dit was die ontwrigting as gevolg van oorlog wat die verspreiding van pokke bevorder het.
Pokke het eers in 1696 in die Suidoos aangekom, anderhalf eeu na die Hernando de Soto -ekspedisie. Daar is eens gedink dat die mans van De Soto pokke dra, maar hierdie siening weerspieël die gebrekkige aanname dat Europeërs altyd met pokke besmet was en altyd aansteeklik was. De Soto se ekspedisie het wel veroorsaak dat siektes in inheemse gemeenskappe ontstaan het, maar die rede was dat die ekspedisie se gewelddadige oorlogvoering gelei het tot uitbrake van patogene, soos disenterie, wat reeds in Amerika was. Toe pokke uiteindelik die Suidoos tref, het dit vinnig versprei van Virginia na Oos -Texas oor netwerke wat deur 'n Engelse handel in inheemse gevangenes geskep is vir slawerny in hul kus- en Wes -Indiese kolonies. Deur menslike liggame aan te val, te vang en te vervoer, het paaie vir die pokkevirus ontstaan. Om die saak te vererger, was die liggame reeds verswak deur oorlog en sy metgeselle - ondervoeding, blootstelling en gebrek aan palliatiewe sorg.
Teen die einde van die 18de eeu was die meeste inheemse gemeenskappe in wat uiteindelik die Verenigde State sou word, aan pokke blootgestel. Namate pokke in die 19de eeu herhaal het, het die impak daarvan egter nie verband gehou met 'n gebrek aan vooraf blootstelling nie, maar met die teenwoordigheid van ongunstige sosiale toestande. Dieselfde toestande sou inheemse gemeenskappe ook vatbaar maak vir 'n magdom ander siektes, waaronder cholera, tifus, malaria, disenterie, tuberkulose, scrofula en alkoholisme. Inheemse kwesbaarheid het - en het - niks te doen met rasse -minderwaardigheid nie, of, sedert die eerste voorvalle, 'n gebrek aan immuniteit, het dit alles te doen met konkrete beleid wat gevolg word deur die Amerikaanse regering, sy state en sy burgers.
Oorweeg die impak van die Indiese verwyderingswet. Hierdie beleid, wat formeel in 1830 aangeneem is, het 'n beroep gedoen op die verskuiwing van inheemse mense oos van die Mississippirivier na 'Indian Territory' (wat uiteindelik Oklahoma en Kansas sou word). Byna almal het van die Cherokee Trail of Tears gehoor, maar dit word selde beskou as 'n gesondheidskrisis wat deur die VSA veroorsaak word. Die uitsetting van die Cherokee uit hul vaderland in Georgia, Noord -Carolina en Tennessee het drie fases gehad. In die eerste het die Amerikaanse weermag Cherokees met geweld uit hul huise gesit en hulle etlike maande in konsentrasiekampe gehou met onvoldoende skuiling, onvoldoende voedsel en geen bron van skoon water nie. Die kampe het doodsstrikke geword. Van die 16 000 mense wat daarin aangehou is, het ongeveer 2 000 gesterf aan dysenterie, kinkhoes, masels en “koors” (waarskynlik malaria). In die tweede fase, die reis na die weste, het 'n ekstra 1,500 omgekom, aangesien mense, wat reeds siek was en verder verswak is deur ondervoeding, trauma en blootstelling, aan verskeie patogene beswyk het. In die maande nadat hulle Oklahoma bereik het - die derde fase - sterf 'n ekstra 500 aan soortgelyke oorsake. Die dodetal was 4 000, oftewel 25 persent van die oorspronklike 16 000 wat uit hul huise gedwing is.
Alhoewel die Cherokee Trail of Tears die bekendste is, was daar tientalle ander sulke gedwonge verwyderings. Creeks, Seminoles, Chickasaws, Choctaws, Senecas, Wyandots, Potawatomis, Sauks and Mesquakies, Ojibwes, Ottawas, Miamis, Kickapoos, Poncas, Modocs, Kalapuyas en Takelmas verteenwoordig slegs 'n gedeeltelike lys van nasies wat spore van trane opgedoen het. Nie almal het dieselfde sterftes as die Cherokee beleef nie, maar baie het dit gedoen, en vir sommige was die tol nog hoër. Die geallieerde Sauks en Mesquakies moes noodgedwonge vier keer uit hul dorpe in die weste van Illinois trek - een keer na die sentrale Iowa, een keer na die westelike Iowa, een keer na Kansas en uiteindelik na Oklahoma. In 1832, die tyd van die eerste uitsetting, was die Sauks en Mesquakies 6 000. Teen 1869, toe hulle uiteindelik na Oklahoma gestuur is, was hul bevolking slegs 900, 'n ontsaglike verlies van 85 persent. Jaar na jaar het onophoudelike siektes, waaronder die uitbreek van pokke in 1851, baie lewens geëis. Lae vrugbaarheid en kindersterfte, as gevolg van wanvoeding, siekte en trauma, het die bevolking vervang. Die Sauk- en Mesquakie -ramp was nie 'n ongeluk nie. Dit was 'n direkte en voorsienbare gevolg van besluite wat deur die Verenigde State en sy burgers geneem is om inheemse mense uit gewenste lande te verdryf en dit na 'n ander plek te skuif.
Navajos (Dinés, soos hulle in hul taal na hulself verwys) is ook uit hul tuislande gesit. In die winter van 1863-1864 het die Amerikaanse weermag verskroeide aarde-taktiek gevolg-hulle perskebome en mielielande vernietig-om hulle na 'n dorre reservaat by Bosque Redondo, aan die Pecosrivier in New Mexico, te dryf. Op die gedwonge optog van 250 myl, bekend as die Long Walk, sterf etlike honderde van die 8 000 tot 9 000 Dinés onderweg. Gedurende die volgende vier jaar het Dinés tot 2500 van hul mense weens siektes en hongersnood verloor. In hul donkerste uur het Diné -leiers egter regeringsamptenare daarin geslaag om hulle uit hul gevangenis te bevry en terug te keer huis toe. Maar al het hul bevolking mettertyd gegroei, bly die nalatenskap van die Long Walk bestaan. Die Diné -historikus Jennifer Denetdale merk op dat “ernstige armoede, verslawing, selfmoord en misdaad op voorbehoude almal hul wortels in die Long Walk het.”
Namate gevalle van COVID-19 einde Maart in die Navajo-reservaat begin verskyn het, het die stampresident Jonathan Nez op Facebook met sy mense gepraat. Hy het herinneringe aan die Long Walk opgeroep, en ''n beroep op die burgers gedoen om mekaar te help', en hulle daaraan te herinner: 'dit was toe die beste uit baie van ons voorvaders gekom het, mekaar gehelp, die vrag vir die ouderlinge gedra, die kinders vir ons gedra moeders. ” 'Nou is dit ons beurt,' het hy gesê, 'om aan ons toekoms, ons kinders, ons kleinkinders te dink.' Deurlopende kolonialisme maak die stryd teen COVID-19 'n uitdaging. Alhoewel die Navajo 'n soewereine nasie is met hul eie hulpbronne, het Dinés 'n hoë voorkoms van toestande - diabetes, hoë bloeddruk en longsiektes - wat hul vatbaarheid verhoog om ernstig siek te word van die koronavirus. Gebrek aan toegang tot skoon water bemoeilik hande was. Baie mense kan nie kos, handreiniger en ander benodigdhede bekostig nie. En daar is 'n akute tekort aan hospitaalbeddens en mediese personeel.
Baie openbare amptenare, gesondheidskundiges en joernaliste vestig die aandag op die onproportionele impak van COVID-19 op kleurgemeenskappe. Tog is groot dele van Amerika onverskillig, indien nie volstrek vyandig nie, om hierdie verskille en die ongelykhede daaronder te erken. Inheemse Amerikaners is baie meer sigbaar vir die algemene publiek as sportmaskotte as as werklike gemeenskappe. Die Trump -administrasie het aanvanklik geweier om verligting aan stamlande te bied in die stimuleringspakket van $ 2 biljoen wat vroeg in April goedgekeur is, en hoewel die wetgewing uiteindelik $ 10 miljard aan stamregerings bewillig het, het die ministerie van finansies, wat die taak gehad het om hierdie fondse te versprei, dit nie uitbetaal nie. Volgens senator Tom Udall in New Mexico, het amptenare van die tesourie "nie weet hoe om op die regte manier met stamme te kommunikeer nie, en kry hulle nie die werk nie."
Die stryd teen die onsigbaarheid van inheemse mense beteken natuurlik 'n groter bewustheid van hoe COVID-19 hulle beïnvloed en 'n groter poging om hulpbronne te verskaf om hulle te help om die huidige uitbraak te bekamp. Dit beteken ook 'n dieper begrip van die geskiedenis van Amerikaanse Indiane en siektes. Alhoewel die maag-grond-epidemie-hipotese moontlik goed bedoel was, bring die fokus op die kort, indien gruwelike, oomblik van aanvanklike kontak siektes veilig na die verre verlede, en gee koloniseerders 'n alibi. Inheemse gemeenskappe veg meer as 'n virus. Hulle stry met die voortgesette nalatenskap van eeue van geweld en onteiening.
Die Groot pokke -epidemie
Elizabeth A. Fenn ondersoek 'n klein bekende katastrofe wat die geskiedenis van 'n kontinent verander het.
Kaptein George Vancouver, wat in 1792 oor die noordwestelike kuslyn van Amerika vaar, was bekommerd. Waar, wonder hy, was al die inboorlinge? Die land was volop, met 'n oënskynlik onbeperkte voorraad salm en vars water, maar daar was opvallend min mense. In plaas daarvan het die Britse seevaarder verlate dorpe gevind. Die eerste wat suid van Vancouver-eiland aan die oewer van Discoverybaai aangetref is, was 'oorloop met onkruid, waaronder verskeie menslike skedels en ander bene, promiskuus versprei'.
Terwyl Vancouver die Straat van Juan de Fuca in kaart bring, herhaal die toneel hom gereeld. 'Tydens hierdie ekspedisie', sê bemanningslid Thomas Manby, 'het ons 'n hele paar verlate dorpe gesien. in staat om baie honderde inwoners te hou. Vir Manby was die gevolgtrekking onvermydelik: 'In elk geval is hierdie land aansienlik ontvol, maar uit watter oorsaak is dit moeilik om vas te stel.' Vancouver stem saam. Al die bewyse, het hy geglo, dui aan 'dat hierdie land op geen baie afgeleë tydstip baie meer bevolk was as tans nie'.
Daar was inderdaad 'n ramp, selfs so groot dat selfs sy getuies en slagoffers nie die omvang daarvan kon waardeer nie. In die jare van 1775 tot 1782, toe die Revolusionêre Oorlog die samelewing en die politiek langs die oostelike kus verander het, het 'n heel ander ramp die hele Noord -Amerikaanse kontinent getref. Die rampspoed, groot en afskuwelik, was pokke.
Word veroorsaak deur 'n matig aansteeklike virus, bekend as Variola major , die aanvanklike tekens van pokke kom twaalf dae na blootstelling, gewoonlik deur infeksie van die asemhalingskanaal. Aanvanklik was die simptome effens soortgelyk aan dié van griep. Dit het hoofpyn, rugpyn, koors, braking en algemene malaise ingesluit. In baie gevalle het slagoffers na die eerste dag of twee beter begin voel, en dikwels gedink dat hulle inderdaad griep gehad het.
Verligting was egter vlugtig. Teen dag vier het die gesig gespoel en die eerste pynlike letsels verskyn - nie op die veloppervlak nie, maar in die mond, keel en neus. Binne vier en twintig uur verskyn die kenmerkende veluitslag. By sommige draai die uitslag na binne, bloeding onder die vel en deur die slymvliese. Hierdie pasiënte sterf vroeg en bloei uit die oë, neus, tandvleis of vagina. By die meeste pasiënte het die pustels egter na die oppervlak van die vel gestoot. As hulle nie saam was nie, was die prognose redelik goed. Maar as die pustels mekaar raakloop in die wat 'samelopende' pokke genoem word, het pasiënte 'n kans van ten minste 60 persent om te sterf.
Namate die uitslag in die mond en keel vorder, het dit moeilik geword om te drink, en dehidrasie het gereeld ingetree. Rondom tien dae, toe die pustels sag geword en blisterig geword het, het baie ontwaterde pasiënte eenvoudig die vloeistof wat hulle bevat, geabsorbeer. Kort daarna, in die woorde van 'n agtiende-eeuse Boston-dokter, het die sere 'begin hardloop en ruik'. Selfs onder higiëniese toestande kan sekondêre bakteriële infeksies heel moontlik intree, met die gevolge heeltemal so ernstig as dié van die pokke. Teen die einde van die tweede week het skurwe begin vorm. In sy beskrywing van pokke onder die Narragansett -Indiane in 1634, beskryf William Bradford hierdie toestand:
. hulle loog op hul harde matte, die pox breek en maak saak, en hardloop mekaar in, hul vel kleef (as gevolg daarvan) aan die matte waarop hulle loog as hulle hulle draai, 'n hele kant sal [f] tegelyk vloei.
Teen week drie het die sterftes skerp afgeneem. Koors het bedaar, en pasiënte het oor die algemeen verbeter namate onooglike littekens letsels en pustels vervang het. Die gewone verloop van die siekte, van die eerste aanvang tot die verlies van alle skurfte, het ongeveer 'n maand geneem. Oorlewendes, hoewel dit dikwels littekens is en in seldsame gevalle selfs deur die siekte verblind is, is ook geseën. Nadat hulle pokke een keer verduur het, was hulle nou immuun. Hulle sou nooit weer die siekte opdoen nie.
Al was dit vreesaanjaend, het die Amerikaners uit die agtiende eeu nie ongewapen pokke in die gesig gestaar nie. Selfs sonder om virologie te verstaan, gebruik hulle twee wapens teen die siekte: isolasie en inenting. Isolasie of kwarantyn beteken eenvoudig om kontak te vermy tussen mense wat siek is met die siekte en mense wat vatbaar is daarvoor. Beddegoed en klere kan spesiale hantering ontvang. Deur kwarantyn korrek gedoen te word, kan verdere besmetting dikwels gestop word. In die koloniale tydperk is isolasie gebruik deur koloniste en inheemse Amerikaners.
Die tweede wapen - selfs nadat Edward Jenner in 1796 inenting gevind het - was inenting. Anders as inenting, wat die koeipokkievirus gebruik het, het inenting die doelbewuste infeksie van 'n vatbare individu met die Variola -virus behels, gewoonlik deur 'n sny in die hand. Om redes wat wetenskaplikes tot vandag toe ontwyk, was ingeëntde pokke in die meeste gevalle baie minder virulent as die 'natuurlike' vorm van die siekte. Oorlewendes het lewenslange immuniteit gewen, net soos deur 'natuurlike' pokke, maar die sterfte was veral laer.
Daar was egter 'n vangs: individue wat onder inenting was, het wel pokke gekry, en hulle was dus ten volle in staat om ander met die siekte te besmet. Tensy die operasie onder streng kwarantyn toegepas word, sou die operasie waarskynlik 'n epidemie veroorsaak as om dit te stop. Om hierdie rede was inenting baie kontroversieel in die Engelse kolonies, waar uitbrake van pokke relatief skaars was. In Engeland was die siekte egter lank reeds endemies, en die prosedure het groter aanvaarding bereik. Hierdie gesamentlike faktore het beteken dat die Britse magte in die vroeë stadiums van die Amerikaanse rewolusie baie meer geneig was as die Amerikaners om immuniteit teen die Variola virus.
Daar was verwoestende uitbrake van pokke sedert die vroeë Spaanse verkenning, maar niemand kan so volledig gedokumenteer word as die epidemie waarvan Vancouver die grimmige oorskot gesien het nie. Die eerste tekens kom tydens die vroeë konflikte van die Amerikaanse Revolusie in 1775-76. In drie verskillende episodes - die beleg van Boston, die beleg van Quebec en die mobilisering van die Ethiopiese regiment van Dunmore - het pokke sy kop opgehef. Uiteindelik het hierdie episodes, veral die eerste twee, generaal George Washington en sy mediese personeel gedwing om belangrike beleidsbesluite te neem rakende pokkebeheer in die kontinentale weermag.
Teen 1775 was die voorlopiges klaar. Die Sugar Act, die Stamp Act, die Tea Party, die Boston Massacre - elkeen het bygedra tot die groeiende skeuring tussen die kolonies en die moederland. Met elke nuwe aksie het vergaderings byeengeroep, skares vergader en boodskappers het heen en weer tussen die kolonies gejaag. Historiese metafore wat beskryf hoe die koloniste 'besmet' raak met 'n 'besmetting van vryheid', lyk dus gepas: toestande was inderdaad perfek vir werklike besmetting.
Epidemiese pokke verskyn eers in Boston, 'n broeikas van revolusionêre ywer. Geïsoleerde voorvalle het in 1774 in omliggende dorpe plaasgevind, maar teen Januarie 1775 het die siekte in Boston self posgevat.
Die eerste slag van die oorlog het in April plaasgevind, en die siekte het gedurende die somer gebly terwyl die kontinentale leër in die stad gevestig was. Om te verhoed dat dit onder hul troepe posvat, het die Amerikaners 'n toegewyde pokkehospitaal in Fresh Pond naby Cambridge opgerig. Op 4 Julie 1775 beveel Washington:
Geen persoon mag na 'n visvangdam of by 'n ander geleentheid na die varswaterdam gaan nie, aangesien daar 'n gevaar kan wees om die pokke in die weermag in te voer.
Elke soldaat wat 'die minste simptome van pokke' toon, het onmiddellike kwarantyn ondergaan.
Die pogings tot beheer was deur die somer suksesvol. Maar in November, toe Bostoniërs binnenshuis draai om die koue van die winter af te weer, het die siekte onder hulle toegeneem. Terselfdertyd het Washington en sy manne te kampe gehad met 'n aansienlike uittog van vlugtelinge uit die geteisterde stad. 'Generaal Howe het 300 inwoners van Boston beveel om Shirley in 'n noodlottige toestand te wys', het Washington aan die kongres geskryf. 'Ek. Ek is vreeslik bang dat hulle die pokke kommunikeer soos dit in Boston voorkom. Hy het die vlugtelinge uit die Amerikaanse kamp verbied.
Toe, in die eerste week van Desember, kom daar vier Britse woestyne met skrikwekkende nuus. Hulle bevelvoerder, generaal William Howe, beweer hulle, het doelbewus vlugtelinge besmet 'met die doel om die pokke onder die troepe te versprei'. Aanvanklik het Washington weinig eer aan die gerug gegee. Maar toe pokke onder die ontheemde Bostoniërs uitbreek, moes die Amerikaners hul pogings om pokke te beheer verdubbel.
Hierdie pogings het vrugte afgewerp. Die siekte het eers onder die Amerikaanse magte versprei nadat die Britte hulle op 17 Maart 1776 onttrek het. Toe, in die nasleep van die beleg, het mense na Boston gestroom. 'Boston', het Moses Morse geskryf, 'het 'n hospitaal geword met die pokke'. Die epidemie het in Julie 'n hoogtepunt bereik.
Die kiesers van die stad, wat wanhopig was om die verspreiding daarvan te beheer, het 'n dramatiese besluit geneem: hoewel inenting tradisioneel in Boston verbied is, het hulle in Julie 'n tydperk van twaalf dae van die verbod afstand gedoen. Die uitgesoekte manne het wagte in die stad geplaas. Niemand wat vatbaar was, kon ingaan nie, niemand met sigbare simptome kon weggaan nie. Uiteindelik, middel September, het die epidemie homself uitgebrand.
Daar was nie sulke goeie nuus van ander fronte nie. Op 6 Mei 1776, na 'n ellendige, vyf maande lange beleg van die Kanadese stad Quebec, het meer as 1500 Amerikaners teen die St Lawrence-rivier gevlug toe 900 Britse stamgaste aan boord gegaan het om die garnisoen in Quebec te verlig. Gedurende die beleg moes die Amerikaners met die Britte en die pokke te kampe gehad het. Terwyl kwarantyn in Boston gewerk het, het dit van die begin af in Quebec misluk. Op 1 Mei 1776, vyf dae voor die terugtog, was 900 van die 1 900 Amerikaanse troepe voor Quebec siek, hoofsaaklik met pokke.
Toe die chaotiese onttrekking op 6 Mei begin, het selfs die skyn van kwarantyn verdwyn: mans in die volle pokke van pokke sukkel deur kniediep sneeu saam met mans wat nog nooit die siekte gehad het nie, terwyl ander nie daarvan bewus was dat hulle pokke broei nie, gemeng met gesonde troepe. ‘My pock had become so sore and troublesome’, soldier Lemuel Roberts recalled, ‘that my clothes stuck fast to my body, especially to my feet and it became a severe trial to my fortitude, to bear my disorder’.
By May 11th, the fleeing soldiers had begun arriving at Sorel, some fifty miles north-east of Montreal, where the Richelieu River enters the St Lawrence. ‘There is Some Regimts all Down in the Small pox not a Single man fit for duty’, wrote one officer on the scene. Among those taken ill was John Thomas, the newly arrived general who had taken charge on May 1st. Thomas relinquished his command on May 21st. By June 1st, he was dead.
Reinforcements now poured into Sorel. The scenes that greeted them were terrifying, and they succumbed to the Variola virus almost as fast as they arrived. On June 11th, General Philip Schuyler wrote to George Washington from Albany, warning him that further reinforcements would ‘rather weaken than strengthen our Army’ unless they had already had smallpox.
By early June, the sight of British sail approaching Sorel had forced the ‘Northern Army’ to continue its retreat along the Richelieu River, eventually pausing at Isle aux Noix near the north entrance of Lake Champlain. Isle aux Noix was hell on earth. ‘My eyes never before beheld such a seen’, wrote John Lacey of Pennsylvania, ‘nor do I ever desire to see such another – the Lice and Maggots seme to vie with each other, were creeping in Millions over the Victims’. Two mass graves consumed thirty to forty bodies per day.
The raging infection caused General John Sullivan to order yet another withdrawal ‘or the Army will be lost, not by the enemy, but by sickness’. And so the army continued southwards to Ticonderoga. At Crown Point in July, the Connecticut painter John Trumbull visited the camp. ‘I did not look into a tent or a hut in which I did not find either a dead or dying man’, he wrote later.
It took until September for the army to cleanse itself. ‘Thank Heaven’, an elated General Horatio Gates wrote to Washington, ‘the small-pox is totally eradicated from amongst us’. The damage is hard to assess, but it is likely that smallpox carried away roughly a thousand men during the Canadian campaign. Returning soldiers, furthermore, launched outbreaks in Connecticut and possibly Pennsylvania.
Native Americans also contracted smallpox during the Quebec invasion, when a British force of Frenchmen and Seneca Indians routed reinforcements sent to the aid of a pox-ridden American garrison at the Cedars. The American patriot John Adams, who bemoaned the general havoc smallpox had created, later noted the results of this episode with satisfaction:
It is some small Consolation that the Scoundrell Savages have taken a large Dose of it. They plundered the Baggage, and stripped off the Cloaths of our Men, who had the Small Pox, out full upon them at the Cedars.
In the months that followed, the disease also appeared further west, striking the Onondaga Iroquois and Indians at Michilimackinac who had assisted in expelling the Americans from Canada.
If the smallpox wreaked havoc on American soldiers retreating from Quebec, their plight remained less poignant than that of a small band of British sympathisers to the south at exactly the same time. The colony was Virginia, where the royal governor, John Murray, Lord Dunmore, had promised freedom to all slaves ‘appertaining to Rebels’ who would fight for the crown. At least 800 African-Americans joined Dunmore, donning uniforms adorned with the words ‘Liberty to Slaves’, and fighting in several skirmishes. But Variola, not patriot Virginians, would be their most formidable enemy.
In February 1776, smallpox appeared among Dunmore’s troops, who had established a precarious camp on a spit of land near Portsmouth, Virginia. By May, nearly 300 had died, and the Governor’s surgeons recommended inoculation. Dunmore decided to leave his vulnerable mainland position and set up an inoculation camp at Gwynn’s Island, where the Piankatank River flows into Chesapeake Bay.
Gwynn’s Island was to Dunmore’s loyalist troops what Isle aux Noix was to the Americans in Canada. An American captive who escaped by swimming to shore in June 1776 claimed that Dunmore lost ‘nine or ten of his black regiment every day by the small pox, &c’.
In July, under a concerted attack by the Virginia rebels, Dunmore and his vastly reduced force gave up the island. Landing within hours of the loyalist departure, the Virginians were appalled at the scene. One described how:
On our arrival, we . were struck with horrour at the number of dead bodies, in a state of putrefaction, strewed all the way from their battery to Cherry-Point, about two miles in length, without a shovelful of earth upon them.
They found ‘others gasping for life and some had crawled to the water’s edge, who could only make known their distress by beckoning to us’. In all, some 500 men had died on the island. The remainder sailed first to the Potomac, and then, in early August, to New York, St Augustine and England. As in the Canadian campaign, returning soldiers and deserters carried smallpox home with them, sparking outbreaks that lasted well into 1777 in tidewater Virginia and Maryland.
In 1777 and 1778, the disease seemed to fade away. In part, the momentary pause in smallpox was due to General Washington’s decision to inoculate the Continental Army. The decision stemmed largely from ‘the deplorable and melancholy situation, to which one of our Armies was reduced last Campaign by the Small pox’ and the certainty that the disease would again take hold if the army was vulnerable. At its core was the recognition that the Revolution had brought about new circumstances in which people and contagious disease circulated rapidly.
So beginning in the spring of 1777 and continuing through the following winter, the American forces went through inoculation at West Point, Morristown, Valley Forge, Alexandria, Dumfries, and Fairfax. The procedure did not always go well for the troops, but quarantine seems to have been secure. There were no complaints of the contagion spreading beyond the designated inoculation sites, and in the difficult Valley Forge winter of 1778, the army managed to keep its temporary debilitation a secret from the British.
The year 1779 was a milestone for smallpox in North America. As the theatre of war moved south, so did the smallpox, primarily affecting civilians, camp followers, and irregular troops in both armies. In early 1779, for example, a combined British force of Waldeckers (German troops) and loyalists from Pennsylvania and Maryland picked up smallpox in Jamaica and carried it to Pensacola Bay.
By mid-October, the disease had reached the Indian town of Little Tallassee, where it ‘reduced them much, and those Towns who have not had it as yet, have fled with their Families into the Woods’. Smallpox also erupted in the cities of Charleston and Savannah, and in the two years that followed, it plagued the southern landscape right along with the war.
Particularly hard hit were the slaves who fled to freedom behind British lines as Cornwallis’s army marched through the south. The retreat to Yorktown, in fact, hearkened back to the Gwynn’s Island epidemic of 1776. But in this instance the British turned their guns on desperately ill African Americans to whom they had promised freedom and instead forced them to return to their masters. Some eyewitnesses believed that this was an attempt to spread smallpox behind the American lines.
But these events paled by comparison to smallpox’s ravages elsewhere. For in 1779, the Variola virus moved westwards, finding its way into the vast susceptible populations it needed to thrive. Now trade, colonial expansion, and the Spanish mission system joined with warfare in transporting and transmitting the disease.
In August 1779, after an eighteen-year hiatus, smallpox struck Mexico City. It moved quickly, and by December 27th the disease had afflicted 44,286 people in the city. ‘A great part of the Mexican youth was cut down that year’, noted the explorer Alexander von Humboldt. By the time it was over, early in 1780, an estimated 18,000 had died.
The virus nevertheless continued to travel. Moving south from Mexico City, the epidemic eventually extended into the South American continent. Traveling north, it arrived in the frontier provinces of Texas and New Mexico in the fall and winter of 1780-81. The historian Hubert Howe Bancroft calculated that in New Mexico alone, the epidemic killed 5,025 mission Indians. If non-mission Indians were included, this number would be much larger.
Even as smallpox ravaged the American southwest and followed Cornwallis’s troops through the southeast, it launched a simultaneous attack on the northern plains and Canadian shield. How did it get there? Very likely by way of the Comanche Indians, the mounted and warlike titans of the southern prairies, who engaged in a spirited horse and slave trade with their Shoshone kinfolk in western Wyoming and Montana.
The great explorer David Thompson recorded the account of an Indian named Saukamappee, who described how, in the summer of 1781, the Piegan Blackfeet had raided a Shoshone village. Knives drawn, the warriors had slashed through their enemies’ tents, and then, Saukamappee said, ‘our war whoop instantly stopt, our eyes were appalled with terror there was no one to fight with but the dead and the dying, each a mass of corruption’. They took no scalps but plundered the village and returned home. Two days later, smallpox broke out.
Before long the disease appeared among the Western Cree and the Assiniboine with whom these Blackfeet traded. On October 22nd, 1781, at a Hudson’s Bay Company post on the North Saskatchewan River, the first Indian turned up with the infection. The man, according to the trader William Walker, had left a tent on the southern prairies
. with Seven Indians laying dead in the Inside that died of the Small pox, and he himself is taken so bad that I believe he never will recover.
Reports of death and disease now poured into the post. Five of Walker’s own men returned from foraging and told of meeting Indians covered with smallpox, trying to cool themselves in the waters of the Eagle River. The dead filled nearby tents, and those who survived ‘were in such a state of despair and despondence that they could hardly converse with us’. From what Walker’s men could discover, ‘three fifths had died under this disease’.
Traders at Fort Vermilion, Portage la Loche, Hudson House, Cumberland House, York Factory, Severn, and Churchill all reported the impact of smallpox in 1781-82. The trading houses of the Canadian Shield, like the missions of the south-west, became deadly centres of contagion, despite the fact that traders often tried to mitigate contact between sick and healthy Indians.
The Shoshones, who were one source of the pestilence that devastated the Canadian interior, appear also to have transmitted the plague to the tribes of the upper Missouri River. Here, in 1805, the explorers Meriwether Lewis and William Clark noted numerous village sites forsaken by the Mandans and Hidatsas ‘about 25 years’ earlier. These towns, Clark said, were ‘destroyed by the Sous [Sioux] & Small Pox’.
The Sioux marauders did not escape unscathed. The surviving evidence does not indicate precisely how the epidemic reached them, but it was very likely in their assaults on the corn-growing Missouri River tribes. The Sioux recorded their fatal encounter with the pestilence in annual chronologies called winter counts. One such count, kept by an Oglala Lakota man named American Horse, designated the year 1780–81 with the simple phrase ‘Many died of smallpox’. In all, the epidemic appears in at least thirteen different winter counts kept by plains Indians in the years 1779–83.
Recorded eyewitness accounts of the pandemic of 1775–82 end at Hudson Bay and the northern plains. The epidemic, however, did not. It struck the northwest coast, where George Vancouver and others observed its depopulating effects.
In 1787, on the coast of what is now south-east Alaska, explorer Nathaniel Portlock spotted what he expected to be a large Tlingit village. But upon landing, he found that only nine people lived there and that the adults bore the marks of smallpox. An animated old man described to Portlock ‘the excessive torments he endured whilst afflicted with the disorder that had marked his face’.
References to abandoned villages and to smallpox-scarred Indians can be found in at least a dozen journals kept on seven different voyages to the Pacific north-west from 1787 to 1795. Even Lewis and Clark, returning through the Cascades in 1806, stopped at a nearly deserted Chinook village where they met an old woman ‘badly marked with the Small Pox’, who remained there still. The woman indicated that the disease had struck ‘about twenty-eight or thirty years past’.
If it is clear that the epidemic did indeed strike the north-west coast, it is not clear exactly how or when it did so. It is most likely that the pox proceeded westward from the Shoshones, following native trade networks down the Columbia River to the sea. Yet no evidence proving this has been found.
It is also possible that the pox arrived by sea. From 1775 to 1779, four Spanish voyages cruised north from San Blas, Mexico, in an effort to stake out and protect territorial claims. Could one of these have carried the infection? Miskien. But if so, it has not yet turned up in the historical record. Nor, for that matter, does mention of smallpox or depopulation appear in the journals of Captain James Cook’s 1778 voyage, perhaps indicating that the epidemic arrived after that date.
Russians also frequented the north-western coastline, and they had already established trading posts in southern Alaska. Smallpox had ravaged Asia’s Kamchatka peninsula in 1768, and there is some evidence that it was present in 1774. But there is no clear indication that Russians carried the contagion eastwards in these years.
We are left, then, with George Vancouver’s mystery. From 1775 to 1782, as conflict and political upheaval rocked the east coast, smallpox had wreaked its own havoc wherever it found access to susceptible populations. From Quebec to Mexico to Hudson Bay, the continent was alive with human activity. Variola found not just susceptible populations, but connections between them. Transported by human carriers between ports and along rivers, roads, lakes, and trails, the virus showed how closely linked seemingly disparate regions already were. In so doing, it forged a horrific common experience that spanned the continent and reshaped life for years to come.
Further Reading:
- Blake, John B. Public Health in the Town of Boston, 1630-1822 ( Harvard UP, 1959)
- Boyd, Robert The Coming of the Spirit of Pestilence: Introduced Infectious Diseases and Population Decline among the Northwest Coast Indians, 1774-1874 (University of Washington Press, 1999)
- Fenn, Elizabeth A. Pox Americana: The Great Smallpox Epidemic of 1775-82 (Hill and Wang, 2001)
- Fenner, F., D. A. Henderson, I. Arita, Z. Ježek, and I. D. Ladnyi Smallpox and Its Eradication (World Health Organization, 1988)
- Roberts, Kenneth, ed. March to Quebec: Journals of the Members of Arnold's Expedition (3rd ed. Doubleday, Doran & Co., 1940)
Elizabeth A. Fenn is an assistant professor of history at Duke University in Durham, North Carolina. Haar Pox Americana (Sutton Publishing, 2003) was joint winner of the Longman-History Today book of the year award 2002.
Smallpox kill Native Americans - History
In the years before English settlers established the Plymouth colony (1616–1619), most Native Americans living on the southeastern coast of present-day Massachusetts died from a mysterious disease. Classic explanations have included yellow fever, smallpox, and plague. Chickenpox and trichinosis are among more recent proposals. We suggest an additional candidate: leptospirosis complicated by Weil syndrome. Rodent reservoirs from European ships infected indigenous reservoirs and contaminated land and fresh water. Local ecology and high-risk quotidian practices of the native population favored exposure and were not shared by Europeans. Reduction of the population may have been incremental, episodic, and continuous local customs continuously exposed this population to hyperendemic leptospiral infection over months or years, and only a fraction survived. Previous proposals do not adequately account for signature signs (epistaxis, jaundice) and do not consider customs that may have been instrumental to the near annihilation of Native Americans, which facilitated successful colonization of the Massachusetts Bay area.
Retrospective studies have inherent, sometimes insurmountable, biases, but speculation on past events by historians and anthropologists is commonplace and offers grist for future studies. We offer an alternative hypothesis for the cause of an epidemic among Native Americans in the years immediately before the arrival of the Pilgrims in Massachusetts. During 1616–1619, many persons died of a disease that presumably spared nearby European fishermen and traders (1). The more severe manifestations were fever, headache, epistaxis, jaundice, and skin lesions. Speculations as to the cause have included plague, yellow fever, and smallpox (2–7), as well as influenza, chickenpox, typhus, typhoid fever, trichinosis, cerebrospinal meningitis, and syndemic infection of hepatitis B virus (HBV) and hepatitis D virus (HDV) (Table 1) (6–11). We propose another disease: leptospirosis, accompanied by Weil syndrome. With its more severe manifestations, this syndrome is consistent with available clinical information, the nidality of Leptospira organisms, the introduction of rodent reservoirs, and the presence of favorable ecologic niches. Practices of the local population placed it repeatedly in high-risk exposures to epidemic and hyperendemic environments.
Epidemiology
The limited information available notes the following clinical manifestations of the illness: headache and fever with visible signs of epistaxis and jaundice. Mode of transmission was not known. Weather and seasonality are unknown, although tree ring data suggest greater than average rainfall in eastern Massachusetts during 1615–1625 (12). The duration of the epidemic (or epidemics) reportedly ranged from 3 to 6 years. Estimated death rates (which lack reliable numerator and denominator data) range from one third of the local population to as high as 90% (1,13). The Patuxet (Plimouth) Native American village was severely depopulated (14). Referring to conditions along the Newfoundland and Maine coasts, where some believe the epidemic may have originated, Pierre Biard, a Jesuit missionary, noted: “They [the Indians] are astonished and often complain that since the French mingle and carry on trade with them, they are dying fast, and the population is thinning out” (15). In New England, Smith noted “three plagues in three years successively neere two hundred miles along the coast” of southern Massachusetts to Cape Cod and inland for 15 miles (16). Bennett suggested a 50–60-mile interior extension, which corresponds to the area of native corn horticulture (17).
Figure 1. Native American tribes of southeastern Massachusetts in ≈1620.
Figure 2. Plymouth, Massachusetts, harbor showing extensive Native American settlement (a sketch by Samuel de Champlain from his voyage of 1606).
By 1616, several subtribes of the Wampanoag (Pokanoket) Nation were living between the present-day borders of eastern Rhode Island and southeastern Maine (Figure 1). The Patuxet village was localized to an area in and around Plymouth harbor (Figure 2). Demographers and historians disagree about the total size of the Wampanoag Nation, but Salisbury considers an estimate of 21,000–24,000 as “not unrealistic for this region” (13). Gookin also estimated 3,000 men living in Massachusetts before the epidemic (18), which when extrapolated for family size is consistent with Salisbury’s overall estimate. Salisbury estimated that the size of the Patuxet tribe before the epidemic was 2,000.
No estimates are available of the number of Portuguese, Breton, and Bristol fishermen Basque whalers French fur traders or English codders who had established a presence on the North Atlantic coast since the early sixteenth century (10). In 1578, an observer noted 100 Spanish sails, 20–30 Basque whalers, ≈150 French and Breton fishing ships, and 50 English sails along the coast of Newfoundland (19). English traders and fishermen had daily contact with indigenous persons but lived on ships or in segregated enclaves on land where salt-dried codfish stations (favored by the English) were built along Massachusetts Bay.
Ekologie
Indigenous ecology was cataloged in 1604 when hundreds of coastal plants, trees, and animals (but not “vermine”) were described (20). Before 1620, there were no peridomiciliary animals except for small dogs and mice (10), although other rodents (e.g., squirrels) were common. Precolonization and postcolonization English written accounts do not mention rats, the numbers of which may have been influenced by the presence of cats, but aboard ships rats must have been common. An earlier explorer noted “Tant qu’on eut des cuirs on ne s’avisa point de faire la guerre aux rats…” (“As long as there is a cargo of skins, it makes no sense to kill the rats.”) (11). The black rat (Rattus rattus) was common in coastal England at the time (yet to be displaced by the brown rat [R. norvegicus] nearly 100 years later) (21) the black rat and mice were universal companions on ships and must have established themselves early on the coastal mainland, seeking harborage in and around Native American households. Once established, rats and mice would become chronic carriers of disease agents, contaminating water and soil and infecting other commensal rodents (e.g., the local mouse Peromyscus leucopus) and other mammals. Fresh and stored food items such as maize, beans, squash, pumpkin, roots, nuts, berries, meat, fish, and shellfish, were also susceptible to leptospiral contamination.
Previous Explanations
One hundred years ago, Williams collected all known information about the epidemic in an article that included 23 primary references, 22 of which contained eyewitness accounts or reports (3). He concluded that the disease may have been bubonic plague and supported his proposal by noting that there were abundant fleas in Indian dwellings, survivors had sores suggestive of buboes, and plague was endemic in London during 1606–1611. Eleven of his 23 primary sources disagreed, as did Carter, who without further elaboration stated that he thought the epidemic was influenza (4). Despite allusions to icterus, Williams discounted yellow fever (as did Carter) he also dismissed other febrile illnesses with jaundice, yet he cited Gookin from 1674: “I have discoursed with old Indians, who were then youths, who say that the bodies all over were exceedingly yellow, describing it by a yellow garment they showed me, both before they died and afterwards.” Trumbull, another eyewitness, noted that the Indian word for the disease meant “a bad yellowing” (3). A recent analysis interpreted it as caused by a confluent form of smallpox (6). Clinical and epidemiologic information about classical explanations and some of the more recent suggestions are summarized in Table 2.
Bespreking
The causes of most historical epidemics may never be proven. The new science of paleomicrobiology may provide some answers, but the question will remain about whether a person died of a specific disease or with the disease. However, even when proper evidence is limited, this limitation should not dissuade speculation about the causes of ancient afflictions. Our hypothesis is not meant to be a definite answer but a heuristic for others to criticize and explore. Alfred Crosby, one of America’s foremost medical historians, coined the term “virgin soil epidemics” to describe immunologically unexposed populations exposed to Old World diseases and cited the 1616–1619 epidemic as an example (9). He also proposed that environmental and behavioral factors were equally important (22). The Massachusetts epidemic supports this observation, and evidence may indicate that “genetic weakness” was not as important as the intimate and repeated exposure to an infectious agent among the Indians not shared by Europeans.
All previously proposed explanations for the epidemic are consistent with an Old World importation into a susceptible population (except for Webster’s, who thought yellow fever was of autochthonous origin). Despite its manifestation and subsequent visitations along coastal America in later years, yellow fever is not a plausible explanation given the routes of the trans-Atlantic slave trade at the time. Transportation of the disease, its vector, and human cargo from Africa to the New World was limited to the Caribbean and Central and South America little evidence exists that any ships visited the New England coast after disembarking slaves (23). Alternative arthropod-borne and other non-arthropod–borne viral hemorrhagic fevers are even less plausible candidates.
Clinical descriptions of other proposed diseases (plague, chickenpox, typhus, typhoid fever, and meningitis) are largely inconsistent with the syndrome described and were dismissed by Bratton. Citing Oliver Wendell Holmes, Sr. (7), Bratton concluded that the disease was smallpox, explaining that the confluent form of pustular smallpox might mimic jaundice (6). In 1799, Webster had discounted smallpox because “the Indians, who were perfectly acquainted with the disease [smallpox] after the English arrived, always gave a very different account of it. ” (2). Two diseases not mentioned by Bratton (trichinosis and HBV/HDV infections) are also unlikely. Pigs were absent in the New World, and the finding of a single pig bone in an undated midden makes a most unlikely explanation for the epidemic. Syndemic HBV/HDV infection presupposes aboriginal HBV carriage, HDV importation, and (in the opinion of Speiss and Speiss) an enteric mode of transmission (8).
In 1886, Adolf Weil originally described a constellation of signs and symptoms that is now eponymic for Weil syndrome (his first patient experienced nasenbluten [nosebleed] on the second day of illness) (24). Inada and Ido identified the causative organism 30 years later (25). Subsequent studies have demonstrated that rodents have high rates of leptospiral carriage and shedding (26). Severe (icteric) leptospirosis was also known as infectious jaundice, epidemic jaundice, and icto-hemorrhagic fever (27). Early outbreaks in the United States were recorded by Neill, including a Union Civil War Surgeon General’s report of a large number of “hepatic and haematic disorders” estimated to have affected >71,000 troops during the War (28).
In 1965, Heath et al. summarized the history of leptospirosis in the United States, analyzing 483 cases reported during 1949–1961 (29,30). Twenty-five percent were caused by L. serovar Icterohemorhagiae. Vandag, L. Icteroheamorrhagiae and other serovars (Canicola, Autumnalis, Hebdomidis, Australis, and Pomona) are endemic in the United States, and isolated instances within the United States continue to be reported (31). More recent reports from the Centers for Disease Control and Prevention (32,33) and ProMED mail (34) demonstrate that leptospirosis is a worldwide, reemerging infection with identifiable risk factors, including immersion in fresh water, exposure to contaminated soil, and antecedent heavy rains (35,36). Unlike hookworm disease, another Old World soil-borne disease that established itself in the more hospitable American South, leptospirosis is a more cosmopolitan fellow traveler and is still recognized as a zoonosis in New England.
Contemporary medical texts conflate signs, symptoms, and death rates of mild leptospiral infection with Weil syndrome, relying on more recent citations in which the nature of exposure, duration, and responsible Leptospira spp. are often not known. Interventional measures (removal from known sources, prompt diagnosis and treatment, and early prevention and control measures) may have decreased overall case-fatality rates and limited the extent of the outbreaks. Nosebleed is rarely mentioned in the recent literature, but “hemorrhages, starting with epistaxis” are noted in a 1944 text on tropical diseases, which also cites high death rates (32% in Europe and 48% in Japan) (27). These surprisingly high death rates in early Japanese reports were attributed to repeated intimate exposure to contaminated water by barefooted mine workers and rice farmers.
Unlike the European experience, epidemics in Japan were rare, and endemic exposures were more common (27). A recent population-based seroepidemiologic study found leptospiral seropositivity rates of 28% in an annually flooded area of the Amazon basin (37). Leptospira spp. were found to cause seasonal outbreaks of a mysterious disease (tentatively named Andaman hemorrhagic fever) during periods of rice paddy sowing and harvesting in the late 1980s on the Andaman Islands in the Indian Ocean (38). Subsequent studies found that leptospiral seroposivity was as high as 62.5% (among agricultural workers) in the Andaman Islands and that the case-fatality rate was 42.9% among hospitalized patients with severe leptospirosis and pulmonary symptoms.
Endemicity and subsequent high case-fatality rates, similar to those reported from Japan, are consistent with a leptospiral etiology for the 1616–1619 epidemic. The Patuxets may not have associated sickness with their environment or traditional ways of living and may have attributed their affliction to many causes, but not to countless exposures and reexposures to the agent. Sporadic, focal mini-epidemics may have played out and coalesced into what was construed as a single “plague” by outside observers. Except for more severe cases of liver failure, the most common cause of death for leptospirosis (renal or respiratory insufficiency) would have not been recognized. The Indian lifestyle, which included constant exposure to rodents and their excreta on land and in water, exposed them to the leptospiral life cycle (Figure 3) (39,40). Bare feet were common in and around houses. Although a rare portal of entry, mucosal exposure may have occurred from ingestion of corn buried in the ground in rodent-accessible baskets and from rodent-contaminated foods in wigwams (weetas). Dermal abrasions offered cutaneous portals of entry. Attendance of the ill and burial of the dead (including those who died from Weil syndrome) would have attracted others who shared local food, water, and camp grounds. It was common practice for entire families to enter sweat lodges followed by immediate immersion in cooling streams and ponds sweat lodges were considered vivifiers and cure-alls for illnesses, a practice that may have reexposed the already ill to contaminated water. Once the spirochete established its presence in numerous foci, it survived for months in water, mud, and moist soil and caused infection in additional mammalian reservoirs. A reduction in the populace may have been incremental, episodic, and continuous daily needs and customs may have exposed the Indians to leptospirosis over many months or years, with only a small fraction of the population eventually surviving. Suggestions that the disease persisted among the Indians after 1619 (perhaps through 1630) support the premise of endemic nidality and selective Indian vulnerability. The fate of nearby European cod fishermen is unknown, but they did not share most of the Indians’ risk factors. Boots would have limited transmission from fresh water exposures, bathing was not a common practice, and work in a saline environment may have curtailed transmission. An occasional case of febrile illness on board ship would have been attributed to many other causes. Disease and death may have occurred among the fishermen but are not recorded.
The exact duration and extent of the epidemic(s) will never be known, but our suggestion offers an alternative explanation. Persistent leptospiral exposures resulted in more severe cases of Weil syndrome and jaundice, a sign that would have been reported by observers the cause of death from other (anicteric) leptospiral infection would not have been recognized. Our proposal is consistent with the historical clinical descriptions, estimated death rates, importation and distribution of its reservoir host, inoculation of the agent in multiple suitable nidalities, spread to other mammalian reservoirs, hyperendemicity, ecologic factors favoring repeated exposure and transmission, and known high-risk activities of the indigenous population.
The name Squanto has entered American history and folklore as the one of the last of the Patuxets who assisted the Pilgrims in 1620. He was one of the few survivors of an epidemic that was crucial to the success of the Plymouth and Massachusetts Bay colonies because remaining Indians had little capacity to resist the new settlers. Two years later, after having fever and a nosebleed, Squanto died of what was then referred to as “the Indean disease.”
Dr Marr is a professor at Virginia Commonwealth University School of Medicine, Richmond, Virginia, and at East Carolina University School of Medicine, Greenville, North Carolina. His research interests include public health history and historical epidemics and diseases.
Mr Cathey is senior editor of the Annals of Saudi Medicine at King Faisal Specialist Hospital, Riyadh, Saudi Arabia, and a professional medical writer. His research interest is historical epidemics.
Acknowledgment
We thank Alfred W. Crosby, Asim A. Jani, Grayson B. Miller, Myron G. Schultz, and Jack Woodall for critical comments Philip McEldowney for literature search/retrieval Stefanie Nauhardt Parker for translation Mariana Ruiz-Villarreal and David Connell for providing the leptospiral life cycle and Reina Tejano and Samuel de Champlain for providing the maps.
Verwysings
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Tables
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Disease can drive human history
Of course, the Aztecs were not the only indigenous people to suffer from the introduction of European diseases. In addition to North America’s Native American populations, the Mayan and Incan civilizations were also nearly wiped out by smallpox. And other European diseases, such as measles and mumps, also took substantial tolls – altogether reducing some indigenous populations in the new world by 90 percent or more. Recent investigations have suggested that other infectious agents, such as Salmonella – known for causing contemporary outbreaks among pet owners – may have caused additional epidemics.
The ability of smallpox to incapacitate and decimate populations made it an attractive agent for biological warfare. In the 18th century, the British tried to infect Native American populations. One commander wrote, “We gave them two blankets and a handkerchief out of the smallpox hospital. I hope it will have the desired effect.” During World War II, British, American, Japanese and Soviet teams all investigated the possibility of producing a smallpox biological weapon.
Mass vaccination against smallpox got going in the second half of the 1800s. Photo courtesy of Everett Historical via Shutterstock.cm
Happily, worldwide vaccination efforts have been successful, and the last naturally occurring case of the disease was diagnosed in 1977. The final case occurred in 1978, when a photographer died of the disease, prompting the scientist whose research she was covering to take his own life.
Many great encounters in world history, including Cortés’s clash with the Aztec empire, had less to do with weaponry, tactics and strategy than with the ravages of disease. Nations that suppose they can secure themselves strictly through investments in military spending should study history – time and time again the course of events has been definitively altered by disease outbreaks. Microbes too small to be seen by the naked eye can render ineffectual even the mightiest machinery of war.
This article was originally published on The Conversation. Read the original article here.
Left: A skeleton discovered at a ruined pyramid in Tlateloco in Mexico City February 10, 2009. Archaeologists have discovered a mass grave with four dozen neatly lined up human skeletons in the heart of Mexico City, revealing clues about the Spanish conquest that killed millions in battle and disease. The 49 bodies, all lying face up with their arms crossed over their chests, were discovered as investigators searched for a palace complex in the Tlatelolco area, once a major religious and political center for the Aztec elite. Photo By Daniel Aguilar/Reuters
