Kopper dræber indianere - historie

Kopper dræber indianere - historie


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Hvor kopper ødelagde aztekerne - og hjalp Spanien med at erobre en amerikansk civilisation for 500 år siden

Richard Gunderman arbejder ikke for, konsulterer, ejer aktier i eller modtager finansiering fra noget selskab eller en organisation, der ville have gavn af denne artikel, og har ikke afsløret relevante tilknytninger ud over deres akademiske udnævnelse.

Partnere

Indiana University yder finansiering som medlem af The Conversation US.

Conversation UK modtager finansiering fra disse organisationer

De seneste udbrud i USA har gjort opmærksom på farerne ved mæslinger. Den Demokratiske Republik Congo bekæmper et dødeligt udbrud af ebola, der har dræbt hundredvis.

Epidemier er naturligvis ikke noget nyt. Og nogle udbredte smitsomme sygdomme har dybt ændret menneskehedens forløb.

For fem hundrede år siden, i februar 1519, sejlede spanieren Hernán Cortés fra Cuba for at udforske og kolonisere aztekernes civilisation i det mexicanske indre. Inden for kun to år var aztekernes hersker Montezuma død, hovedstaden Tenochtitlan blev taget til fange, og Cortés havde krævet aztekernes rige for Spanien. Spansk våben og taktik spillede en rolle, men størstedelen af ​​ødelæggelsen blev udført af epidemier af europæiske sygdomme.


Tidlig kontrolindsats

Kopper var en frygtelig sygdom. I gennemsnit døde 3 ud af hver 10 mennesker, der fik det. Folk, der overlevede, havde normalt ar, som nogle gange var alvorlige.

En af de første metoder til bekæmpelse af kopper var variolation, en proces opkaldt efter virussen, der forårsager kopper (variola -virus). Under variolation blev mennesker, der aldrig havde haft kopper, udsat for materiale fra kopper (pustler) ved at ridse materialet i armen eller indånde det gennem næsen. Efter variolation udviklede folk normalt symptomerne forbundet med kopper, såsom feber og udslæt. Men færre mennesker døde af variolation, end hvis de havde erhvervet kopper naturligt.

Grundlaget for vaccination begyndte i 1796, da den engelske læge Edward Jenner lagde mærke til, at mælkepiger, der havde fået koer, var beskyttet mod kopper. Jenner kendte også til variolation og gættede på, at udsættelse for kopper kunne bruges til at beskytte mod kopper. For at afprøve sin teori tog Dr. Jenner materiale fra en koeboks øm på mælkepigen Sarah Nelmes & rsquo-hånd og podede det i armen på James Phipps, den 9-årige søn af Jenner & rsquos gartner. Måneder senere udsatte Jenner Phipps flere gange for variola -virus, men Phipps udviklede aldrig kopper. Flere eksperimenter fulgte, og i 1801 offentliggjorde Jenner sin afhandling & ldquoOn the Origin of the Vaccine Inoculation. være det endelige resultat af denne praksis. & rdquo

Vaccination blev bredt accepteret og erstattede gradvist variolation. På et tidspunkt i 1800 -tallet ændrede virussen sig til at få koppevaccinen til at skifte fra kopper til vacciniavirus.

Spor af kopper pustler fundet på hovedet på den 3000-årige mumie af Farao Ramses V. Foto med tilladelse fra Verdenssundhedsorganisationen (WHO)

Edward Jenner (1749 & ndash1823). Foto med tilladelse fra National Library of Medicine.


Vaccinationsejr

Den menneskelige kamp mod kopper går cirka 2000 år tilbage. I Asien involverede en teknik kendt som variolation bevidst infektion af en person ved at blæse tørrede kopper skorper op i deres næse. Dem, der modtog denne behandling, fik en mild form for sygdommen og udviklede en livslang immunitet.

Et vigtigt gennembrud kom i 1796, da et eksperiment af den engelske læge Edward Jenner viste, at inokulering ved hjælp af nært beslægtede køer kunne beskytte mod kopper. Jenners opdagelse banede vejen for senere vaccinationsprogrammer - især afgørende, da der ikke er nogen effektiv behandling af kopper.

I 1967, et år hvor cirka 10 millioner til 15 millioner mennesker blev ramt af kopper, lancerede Verdenssundhedsorganisationen en verdensomspændende udryddelseskampagne baseret på vaccination. Efterhånden blev sygdommen skubbet tilbage til Afrikas Horn, og det sidste kendte naturlige tilfælde opstod i Somalia i 1977.


Gav tidlige europæiske opdagelsesrejsende virkelig indfødte amerikanere kopper-inficerede tæpper?

Hvis de stillede spørgsmålet: Gav tidlige europæiske opdagelsesrejsende virkelig indfødte amerikanere kopper-inficerede tæpper ?, ville de fleste synes, at spørgsmålet var latterligt. Det er dog muligvis ikke så langt hentet. Om der rent faktisk er sket eller ej, åbnes for debat, men der er tilstrækkeligt bevis til at vise, at den nøjagtige handling blev overvejet som et krigsværktøj mod indianere.

Koppernes historie
Det første kendte tilfælde af kopperne fandt sted i 1507 på øen Hispaniola. Denne ø er i dag kendt som Haiti og Den Dominikanske Republik. Mange mener, at det var den spanske opdagelsesrejsende Herman Cortes og 600 soldater, der brugte sygdommen til at besejre millioner af azteker i 1520. Kopper kom sandsynligvis til Amerika via pilgrimme, der landede i Massachusetts. I midten af ​​1700 -tallet havde kopper spredt sig klart over landet. Da sygdommen kan leve af klud eller i støv i lange perioder, spredte den sig så hurtigt, at den krediteres med at udslette 30% af alle de indianere, der blev smittet. Kopper kan også have spillet en rolle i udryddelsen af ​​Taino på Bahamas og Større Antiller.

Kopperplanen
I 1763 var de britiske styrker engageret i kamp med Ottawa -stammen under Pontiac ’s oprør. Ifølge dokumenter opdaget af Peter d ’Errico, professor i juridiske studier ved University of Massachusetts i Amherst, sendte Lord Jeffrey Amherst, chef for britiske styrker i Nordamerika, angiveligt et brev til oberst Henry Bouquet. I dette brev diskuterede han tilsyneladende muligheden for at inokere indianerne med kopper ved brug af tæpper. Dette faktiske brev er nogensinde blevet opdaget, men anden korrespondance mellem Amherst og Bouquet indikerede bestemt eksistensen af ​​et sådant brev.

Blev planen gennemført?
Svaret på dette spørgsmål er, at ingen rigtig ved det. Det man ved er, at det var muligt, da der var tæpper til rådighed i Fort Pitt, hvor sygdommen for nylig var blevet opdaget. Den anden faktor, der gør en så vanvittig plan mulig, var Amhersts opfattelse af den indianske indianer som noget på niveau med en hund. Han havde angivet, at han troede, det var spild af gode mænd at gå efter disse dyr (Ottawa) og havde ledt efter måder at eliminere dem på uden at risikere hans mænds liv. Han refererede endda til at kopiere de samme metoder, som spanskerne havde brugt til at besejre aztekerne.

Så hvad er svaret på spørgsmålet. Gav tidlige europæiske opdagelsesrejsende virkelig indianere kopper-inficerede tæpper? Sandheden er ukendt, men deres omstændighedsbeviser er tilstrækkelige nok til at komme med en rimelig påstand. Den britiske officer talte om muligheden for faktisk at gøre det, tæpper var til rådighed, den snydende tankegang var på plads, og mange indianere døde af sygdommen. Det er sådan en djævelsk opfattelse, at de fleste mennesker finder det uforståeligt. Men faktum er stadig, det var krigstider, og de britiske soldater var i krig.


Version 1: 1992

Churchill udgav den tidligste kendte iteration af hans kopper tæppe fabel i 1992, som et kapitel i en bog redigeret af M. Annette Jaimes, som var Churchills kone på det tidspunkt. Kapitlets forfatterskab blev imidlertid skitseret til "Lenore A. Stiffarm with Phil Lane, Jr." De ser ud til at være rigtige mennesker. I 2006 hævdede han, som en del af Churchills forsvar mod anklager om plagiat, at han havde spøget skrevet dette kapitel (Wesson et al., 2006, s. 40, fn. 78). University of Colorado's undersøgelsesudvalg for forskningsfejl accepterede Churchills ghostwriting -påstand til pålydende værdi. Kapitlet bærer faktisk Churchills stilistiske tics og replikerer de opdigtede detaljer, Churchill ville fortsætte med at genudgive under sit eget navn seks gange mere.

Imidlertid gjorde Churchill sårbar over for nye anklager om fabrikation og forfalskning med hensyn til hans kopper tæppe fortælling. Kapitlet "Stiffarm and Lane" (1992) hævder, at:

Ganske vist var fordelingen af ​​kopper-inficerede tæpper af den amerikanske hær til Mandans ved Fort Clark, ved Missouri-floden i nutidens South Dakota, forårsagende for pandemien 1836-1840. (s. 32)

"Stiffarm og Lane's" slutnote lyder:

Tæpperne blev taget fra en amerikansk hærs hospital i St. Louis og sendt op ad floden på damperen St. Peter's. De blev fordelt af hærspersonale den 19. juni 1837. Se Chardon, Francis A., Journal at Fort Clark, 1834-39, State Historical Society of South Dakota, Pierre, 1932. (s. 50, fn. 55)

Sikkert skjult bag en falsk byline, lancerer Churchill et ad hominem -angreb på Russell Thornton, forfatteren, hvis dødelighed anslår, at Churchill støtter sig til sin kopper tæppe fabel. I dække af "Stiffarm og Lane" betegner Churchill Thornton som "en lidt forvirret Cherokee -demograf. Der ser ud til at have skimtet en mulighed for at erhverve 'akademisk troværdighed' ved at tilføre vægten af ​​sin 'native voice' til koret af 'respektable lærdes [.] "(s. 27).


Sygdom har aldrig været bare sygdom for indianere

Indfødte samfunds sårbarhed over for epidemier er ikke en historisk ulykke, men et direkte resultat af undertrykkende politik og vedvarende kolonialisme.

Om forfatteren: Jeffrey Ostler er Beekman -professor i nordvest- og stillehavshistorie ved University of Oregon. Han er forfatter til Overlevende folkedrab: Native Nations og USA fra den amerikanske revolution til blødende Kansas.

Da dødstallet fra COVID-19 stiger, har farvede mennesker tydeligvis større risiko end andre. Blandt de mest sårbare er indianere. For at forstå, hvor skrækkelig COVID-19-situationen bliver for disse samfund, skal du overveje situationen, der udspiller sig for Navajo Nation, et folk med hjemland i Arizona, New Mexico og Utah. Den 23. april var der rapporteret 1.360 infektioner og 52 dødsfald blandt Navajo Reservations 170.000 mennesker, en dødelighed på 30 pr. 100.000. Kun seks stater har en højere vejafgift pr.

Spredningen af ​​COVID-19 minder om tidligere sygdomsudbrud, der har hærget indianersamfund. Mange af disse udbrud resulterede i katastrofalt tab af liv, langt større end endda de værst tænkelige scenarier for COVID-19. Selv influenzapandemien fra 1918-1919, hvor anslået 650.000 amerikanere døde (0,6 procent af 1920 -befolkningen på 106 millioner), blegner i sammenligning med de tab indianere har lidt af sygdom.

Indtil for nylig har sygdomshistorier og indianere lagt vægt på "jomfru-jordepidemier." Ifølge denne teori, populær i Jared Diamond's Kanoner, kim og stål, da europæerne ankom til den vestlige halvkugle, bragte de sygdomme (især mæslinger og kopper), som oprindelige mennesker aldrig havde oplevet. Fordi de ikke havde immunitet over for disse sygdomme, så teorien siger, tog de resulterende epidemier livet af 70 procent eller mere af den indfødte befolkning i hele Amerika.

Ny forskning giver imidlertid et meget mere kompliceret billede af sygdom i amerikansk indisk historie. Denne forskning viser, at jomfru-jordepidemier ikke var så almindelige som tidligere antaget og flytter fokus til, hvordan sygdomme gentagne gange angreb indfødte samfund i årtier og århundreder efter Europæerne ankom først. Postkontaktsygdomme lammede ikke så meget, fordi oprindelige folk manglede immunitet, men fordi betingelserne skabt af europæisk og amerikansk kolonialisme gjorde indfødte samfund sårbare. Jomfru-jord-epidemiens hypotese var værdifuld til at imødegå tidligere teorier, der tilskriver indfødt amerikansk tilbagegang til racemæssig underlegenhed, men dens enestående vægt på biologisk forskel indebar, at befolkningskollaps ikke var andet end historiske ulykker. Ved at understrege betydningen af ​​sociale forhold, der skabes af menneskelige beslutninger og handlinger, giver det nye stipendium et langt mere foruroligende billede. Det hjælper os også med at forstå de problemer, indfødte samfund står over for i dag, når de bekæmper den nye coronavirus.

Jomfru-jordepidemier opstod uden tvivl. I 1633 ramte for eksempel en koppe -epidemi indfødte samfund i New England, hvilket reducerede befolkningen i Mohegan og Pequot fra i alt 16.000 til kun 3.000. Epidemien spredte sig til Haudenosaunee i New York, men ikke længere mod vest end det. Kopper ramte ikke samfund i Ohio Valley og Great Lakes før 1756–57, et århundrede eller mere efter første kontakt med europæere. Da det gjorde det, var det fordi indfødte krigere, rekrutteret til at kæmpe for franskmændene mod briterne under syvårskrigen, havde smittet virussen i øst og inficeret deres lokalsamfund, da de vendte hjem. Manglende immunitet havde betydning, men det var forstyrrelsen som følge af krig, der fremmede koppernes spredning.

Kopper ankom først i Sydøst i 1696, halvandet århundrede efter Hernando de Soto -ekspeditionen. Man troede engang, at de Sotos mænd bar kopper, men denne opfattelse afspejlede den mangelfulde antagelse om, at europæere altid var smittet med kopper og altid smittede. De Sotos ekspedition fik sygdom til at bryde ud i indfødte samfund, men årsagen var, at ekspeditionens voldelige krigsførelse førte til udbrud af patogener såsom dysenteri, som allerede var til stede i Amerika. Da kopperne endelig ramte Sydøst, spredte den sig hurtigt fra Virginia til Øst -Texas på tværs af netværk skabt af en engelsk handel med indfødte fanger til slaveri i deres kyst- og vestindiske kolonier. Raiding, indfangning og transport af menneskelige kroppe skabte veje til koppevirus. For at gøre tingene værre var disse kroppe allerede svækket af krig og dets ledsagere - underernæring, udsættelse og mangel på palliativ pleje.

I slutningen af ​​1700 -tallet havde de fleste indfødte samfund i det, der i sidste ende ville blive USA, været udsat for kopper. Ikke desto mindre, da kopperne gentog sig i det 19. århundrede, korrelerede dens indvirkning ikke med mangel på tidligere eksponering, men med tilstedeværelsen af ​​ugunstige sociale forhold. Disse samme forhold ville også gøre indfødte samfund modtagelige for en lang række andre sygdomme, herunder kolera, tyfus, malaria, dysenteri, tuberkulose, scrofula og alkoholisme. Indfødt sårbarhed havde - og har - intet at gøre med racemæssig mindreværd, eller siden de første hændelser, mangel på immunitet snarere, har det alt at gøre med konkrete politikker ført af den amerikanske regering, dens stater og dets borgere.

Overvej virkningen af ​​den indiske fjernelseslov. Formelt vedtaget i 1830 opfordrede denne politik til flytning af oprindelige folk øst for Mississippi -floden til "Indian Territory" (hvad der i sidste ende ville blive Oklahoma og Kansas). Næsten alle har hørt om Cherokee Trail of Tears, men det betragtes sjældent som en USA-forårsaget sundhedskrise. Udvisningen af ​​Cherokee fra deres hjemland i Georgia, North Carolina og Tennessee havde tre faser. I den første udsatte den amerikanske hær tvangs -cherokeer fra deres hjem og holdt dem i flere måneder i koncentrationslejre med utilstrækkeligt husly, utilstrækkelig mad og ingen kilde til rent vand. Lejrene blev dødsfælder. Af de 16.000 mennesker, der blev holdt i dem, døde omkring 2.000 af dysenteri, kighoste, mæslinger og "feber" (sandsynligvis malaria). I den anden fase, rejsen mod vest, døde yderligere 1.500, da mennesker, der allerede var syge og yderligere svækket af fejlernæring, traumer og udsættelse, bukkede under for flere patogener. I månederne efter at have nået Oklahoma - den tredje fase - døde yderligere 500 af lignende årsager. Dødstallet var 4.000 eller 25 procent af de oprindelige 16.000 tvunget fra deres hjem.

Selvom Cherokee Trail of Tears er den mest kendte, var der snesevis af andre sådanne tvangsfjernelser. Creeks, Seminoles, Chickasaws, Choctaws, Senecas, Wyandots, Potawatomis, Sauks and Mesquakies, Ojibwes, Ottawas, Miamis, Kickapoos, Poncas, Modocs, Kalapuyas og Takelmas repræsenterer kun en delvis liste over nationer, der led af tårer. Ikke alle oplevede den samme dødelighed som Cherokee, men mange gjorde det, og for nogle var vejafgiften endnu højere. De allierede Sauks og Mesquakies blev tvunget til at flytte fire gange fra deres landsbyer i det vestlige Illinois - en gang til det centrale Iowa, en gang til det vestlige Iowa, en gang til Kansas og til sidst til Oklahoma. I 1832, tidspunktet for den første udvisning, talte Sauks og Mesquakies 6.000. I 1869, da de endelig blev sendt til Oklahoma, var deres befolkning kun 900, et svimlende tab på 85 procent. År efter år tog utrættelige sygdomme, herunder et udbrud af kopper i 1851, mange liv. Lav fertilitet og spædbarnsdødelighed som følge af fejlernæring, sygdom og traumer hindrede befolkningsudskiftning. Sauk- og Mesquakie -katastrofen var ikke en ulykke. Det var en direkte og forudsigelig konsekvens af beslutninger truffet af USA og dets borgere om at fordrive indfødte i ønskværdige lande og skubbe dem et andet sted.

Navajos (Dinés, som de omtaler sig selv på deres sprog) blev også smidt ud af deres hjemland. I vinteren 1863–64 forfulgte den amerikanske hær taktisk med brændt jord-ødelægger deres ferskentræer og kornmarker-for at køre dem til et ufrugtbart reservat ved Bosque Redondo, ved Pecos-floden i New Mexico. På den tvungne march på 250 kilometer, kendt som Long Walk, døde flere hundrede af de 8.000 til 9.000 Dinés undervejs. I løbet af de næste fire år mistede Dinés hele 2.500 af deres folk til sygdom og sult. I deres mørkeste time sejrede Diné -ledere dog med succes over for embedsmænd at frigive dem fra deres fængsel og vende hjem. Men selvom deres befolkning er vokset med tiden, forbliver arven fra Long Walk. Diné -historikeren Jennifer Denetdale bemærker, at "alvorlig fattigdom, afhængighed, selvmord og kriminalitet på forbehold alle har deres rødder i Long Walk."

Da tilfælde af COVID-19 begyndte at dukke op på Navajo-reservatet i slutningen af ​​marts, talte stammepræsident Jonathan Nez til sit folk på Facebook. Han kaldte på minderne om den lange gåtur, "opfordrede borgerne til at hjælpe hinanden" og mindede dem "det var dengang, det bedste kom ud af mange af vores forfædre, hjalp hinanden, bar byrden for de ældste, bar børnene til vores mødre. ” "Nu er det vores tur," sagde han, "til at tænke på vores fremtid, vores børn, vores børnebørn." Løbende kolonialisme gør bekæmpelse af COVID-19 til en udfordring. Selvom Navajo er en suveræn nation med egne ressourcer, har Dinés en høj forekomst af sygdomme - diabetes, hypertension og lungesygdomme - der øger deres modtagelighed for at blive alvorligt syg af coronavirus. Manglende adgang til rent vand gør håndvask vanskelig. Mange mennesker har ikke råd til mad, håndsprit og andre fornødenheder. Og der er en akut mangel på hospitals senge og medicinsk personale.

Mange offentlige embedsmænd, sundhedseksperter og journalister henleder opmærksomheden på den uforholdsmæssige indvirkning af COVID-19 på farvesamfund. Alligevel er store segmenter i Amerika ligeglade, hvis ikke direkte fjendtlige, over for at genkende disse forskelle og de uligheder, der ligger til grund for dem. Indianere er synlige for offentligheden langt oftere som sportsmascotter end som egentlige fællesskaber. Trump -administrationen modstod oprindeligt nogen form for lettelse til stammefolk i den stimuleringspakke på 2 billioner dollars, der blev vedtaget i begyndelsen af ​​april, og selvom lovgivningen i sidste ende bevilgede 10 milliarder dollar til stammeregeringer, har finansministeriet, der har til opgave at fordele disse midler, ikke formået at betale dem ud. Ifølge New Mexico senator Tom Udall ved embedsmænd i finansministeriet "ikke, hvordan de skal interagere på passende måde med stammer, og de får bare ikke arbejdet udført."

Modvirkning af urfolks usynlighed betyder naturligvis større bevidsthed om, hvordan COVID-19 påvirker dem og øget indsats for at skaffe ressourcer til at hjælpe dem med at bekæmpe det nuværende udbrud. Det betyder også at skabe en dybere forståelse af historien om amerikanske indianere og sygdomme. Selv om den jomfru-jord-epidemiske hypotese kan have været velment, har dens fokus på det korte, om end forfærdelige øjeblik af første kontakt, overført sygdom sikkert til den fjerne fortid og giver kolonisatorer et alibi. Indfødte samfund kæmper mere end en virus. De kæmper med den igangværende arv fra århundreders vold og bortskaffelse.


Den store koppepidemi

Elizabeth A. Fenn undersøger en lidt kendt katastrofe, der omformede historien om et kontinent.

På sejltur på den nordvestlige kyst i Amerika i 1792 var kaptajn George Vancouver bekymret. Hvor, undrede han sig, var alle de indfødte? Landet var rigeligt, med en tilsyneladende ubegrænset forsyning af laks og ferskvand, men der var påfaldende få mennesker. I stedet fandt den britiske navigatør øde landsbyer. Den første, der stødte på syd for Vancouver Island ved bredden af ​​Discovery Bay, var 'overkørt med ukrudt, blandt hvilke der blev fundet flere menneskelige kranier og andre knogler, promiskuøst spredt rundt'.

Da Vancouver kortlagde Juan de Fuca -strædet, gentog scenen sig regelmæssigt. 'Under denne ekspedition' bemærkede besætningsmedlem Thomas Manby, 'vi så rigtig mange øde landsbyer nogle af dem. i stand til at rumme mange hundrede indbyggere. For Manby var konklusionen uundgåelig: ’Under et eller andet tilfælde er dette land blevet affolket betydeligt, men af ​​hvilken årsag er det svært at afgøre.’ Vancouver var enig. Alle beviserne, mente han, indikerede 'at dette land på ingen meget fjerntliggende periode havde været langt mere folkerigt end i øjeblikket'.

Der havde virkelig været en katastrofe, en så stor, at selv dens vidner og ofre ikke kunne sætte pris på dens omfang. I årene fra 1775 til 1782, da revolutionskrigen omformede samfund og politik langs den østlige kyst, rystede en meget anderledes katastrofe hele det nordamerikanske kontinent. Katastrofen, enorm og frygtelig, var kopper.

Forårsaget af en moderat smitsom virus kendt som Variola major , de første tegn på kopper kom tolv dage efter eksponering, normalt ved infektion i luftvejene. De første symptomer var milde i starten, og de lignede meget influenza. De omfattede hovedpine, rygsmerter, feber, opkastning og generel utilpashed. I mange tilfælde begyndte ofre at føle sig bedre efter den første dag eller to og troede ofte, at de virkelig havde lidt en influenza.

Lettelse var imidlertid flygtig. På dag fire skyllede ansigtet og de første smertefulde læsioner dukkede op - ikke på overfladen af ​​huden, men i munden, halsen og næsepassagerne. Inden for fireogtyve timer dukkede det markante hududslæt op. På nogle vendte udslættet indad og blødede under huden og gennem slimhinderne. Disse patienter døde tidligt og blødte fra øjne, næse, tandkød eller skede. På de fleste patienter skubbede pustlerne imidlertid til hudens overflade. Hvis de ikke løb sammen, var prognosen rimelig god. Men hvis pustlerne løb ind i hinanden i det, der blev kaldt 'sammenflydende' kopper, havde patienterne mindst 60 procent chance for at dø.

Efterhånden som udslættet skred frem i munden og halsen, blev det svært at drikke, og dehydrering begyndte ofte. Omkring dag ti, når pustlerne blev blødere og blærede, absorberede mange dehydrerede patienter simpelthen den væske, de indeholdt. Kort tid efter begyndte sårene med ordene fra en Boston-læge fra det attende århundrede at 'knække løb og lugte'. Selv under hygiejniske forhold kan sekundære bakterieinfektioner godt komme til, med konsekvenser lige så alvorlige som kopperne. Ved slutningen af ​​den anden uge begyndte der at danne skorper. I sin beskrivelse af kopper blandt Narragansett -indianerne i 1634 beskrev William Bradford denne tilstand:

. de lutter på deres hårde måtter, poxet går i stykker og betyder noget, og kører ind i hinanden, deres hud klæber (af årsag hertil) til de måtter, de lutter på, når de vender dem, en hel side vil loppe af [f] på en gang.

I uge tre faldt dødeligheden kraftigt. Feberen aftog, og patienterne blev generelt bedre, da grimme ar erstattede skorper og pustler. Det sædvanlige forløb af sygdommen, fra den første begyndelse til tabet af alle skorper, tog cirka en måned. Overlevende, selvom de ofte var arret og i sjældne tilfælde endda blindet af sygdommen, blev også velsignet. Efter at have udholdt kopper en gang, var de nu immune. De ville aldrig fange sygdommen igen.

Selvom det var frygtindgydende, stod amerikanere fra det attende århundrede ikke over for kopper ubevæbnet. Selv uden en forståelse af virologi anvendte de to våben mod sygdommen: isolation og podning. Isolering eller karantæne betød simpelthen at undgå kontakt mellem personer, der var syge med sygdommen, og personer, der var modtagelige for den. Sengetøj og tøj modtager muligvis særlig håndtering. Udført korrekt kan karantæne ofte standse yderligere smitte. I kolonitiden blev isolation brugt af kolonister og indianere.

Det andet våben - anvendt selv efter Edward Jenners opdagelse af vaccination i 1796 - var podning. I modsætning til vaccination, der udnyttede ko -koppevirus, involverede podning den bevidste infektion af et modtageligt individ med Variola -virus, normalt gennem et snit på hånden. Af grunde, der undviger forskere den dag i dag, var inokuleret kopper i de fleste tilfælde meget mindre virulent end den 'naturlige' form af sygdommen. Overlevende vandt livslang immunitet, ligesom de ville fra 'naturlig' kopper, men dødeligheden var især lavere.

Der var imidlertid en fangst: individer under podning kom ned med kopper, og de var derfor fuldt ud i stand til at inficere andre med sygdommen. Medmindre det blev praktiseret under streng karantæne, var operationen lige så tilbøjelig til at starte en epidemi som at stoppe en. Af denne grund var podning meget kontroversiel i de engelske kolonier, hvor udbrud af kopper var forholdsvis sjældne. I England havde sygdommen imidlertid længe været endemisk, og proceduren opnåede bredere accept. Disse kombinerede faktorer betød, at de britiske styrker i de tidlige stadier af den amerikanske revolution var langt mere tilbøjelige end amerikanerne til at have opnået immunitet over for Variola virus.

Der havde været ødelæggende udbrud af kopper fra tidspunktet for tidlig spansk udforskning, men ingen kan dokumenteres så fuldstændigt som den epidemi, som Vancouver havde glimt af de dystre rester. De første tegn kom under de tidlige konflikter i den amerikanske revolution i 1775-76. I tre forskellige episoder - belejringen af ​​Boston, belejringen af ​​Quebec og mobilisering af Dunmores etiopiske regiment - rejste kopperne hovedet. Til sidst skubbede disse episoder, især de to første, general George Washington og hans medicinske personale til at træffe vigtige politiske beslutninger vedrørende kopperbekæmpelse i den kontinentale hær.

I 1775 var forberedelserne færdige med. Sugar Act, Stamp Act, Tea Party, Boston Massacre - hver havde bidraget til den voksende kløft mellem kolonierne og moderlandet. For hver ny aktion indkaldtes der til møder, skarer samledes, og budbringere løb frem og tilbage mellem kolonierne. Historiske metaforer, der beskriver kolonisterne, der bliver 'smittet' med en 'frihedssmitte' synes derfor passende: forholdene var virkelig perfekte til egentlig smitte.

Epidemisk kopper dukkede først op i Boston, der var et arnested for revolutionær glød. Isolerede hændelser havde fundet sted i de omkringliggende byer i 1774, men i januar 1775 havde sygdommen taget fat i selve Boston.

Krigens første kamp fandt sted i april, og sygdommen fester sig gennem sommeren, mens den kontinentale hær var forankret rundt i byen. For at forhindre det i at tage fat blandt deres tropper, oprettede amerikanerne et dedikeret koppehospital ved Fresh Pond nær Cambridge. Den 4. juli 1775 beordrede Washington:

Ingen må have lov til at tage til Ferskvandsdam for at fiske eller ved en anden lejlighed, da der kan være fare for at indføre småkopper i hæren.

Enhver soldat, der viste 'de mindste symptomer på småkopper', stod over for øjeblikkelig karantæne.

Bestræbelserne på at kontrollere var vellykkede gennem sommeren. Men i november, da bostoniere vendte indendørs for at afværge vinterens kulde, steg sygdommen blandt dem. På samme tid måtte Washington og hans mænd kæmpe med en betydelig flygtning af flygtninge fra den ramte by. 'General Howe har beordret 300 indbyggere i Boston til at pege Shirley i nødlidende tilstand', skrev Washington til kongressen. ’Jeg. er under frygtelig frygt for deres kommunikation af kopperne, som det er udbredt i Boston '. Han forbød flygtningene fra den amerikanske lejr.

Derefter, i den første uge i december, ankom fire britiske desertører med skræmmende nyheder. Deres kommandør, general William Howe, hævdede de, havde bevidst inficeret flygtninge 'med et design for at sprede Småkopper blandt Tropperne'. I første omgang gav Washington lidt rygte til rygterne. Men da kopper brød ud blandt de fordrevne bostoniere, blev amerikanerne tvunget til at fordoble deres indsats for at bekæmpe kopper.

Disse bestræbelser gav pote. Sygdommen spredte sig først blandt de amerikanske styrker, efter at briterne trak sig tilbage den 17. marts 1776. Derefter strømmede folk i kølvandet på belejringen ind i Boston. 'Boston', skrev Moses Morse, 'er blevet et hospital med småkopper'. Epidemien toppede i juli.

Desperat efter at kontrollere dens spredning tog byens udvalgte mænd en dramatisk beslutning: selvom podning traditionelt var forbudt i Boston, afstod de fra forbuddet i en periode på tolv dage i juli. De udvalgte mænd sendte vagtposter rundt i byen. Ingen modtagelige kunne komme ind, ingen med synlige symptomer kunne forlade. Endelig, i midten af ​​september, brændte epidemien sig selv ud.

Der var ingen sådanne gode nyheder fra andre fronter. Den 6. maj 1776 efter en elendig fem måneders belejring af den canadiske by Quebec flygtede mere end 1.500 amerikanere op ad St Lawrence-floden, da 900 britiske stamgæster gik i land for at aflaste Quebec-garnisonen. Gennem belejringen havde amerikanerne måttet kæmpe med både briterne og kopperne. Mens karantæne havde arbejdet i Boston, mislykkedes det fra starten i Quebec. Den 1. maj 1776, fem dage før tilbagetrækningen, var 900 af de 1.900 amerikanske tropper før Quebec syge, primært med kopper.

Da den kaotiske tilbagetrækning begyndte den 6. maj, forsvandt endda karantæneens udseende: mænd i fuld kopper kæmpede gennem knæ-dyb sne sammen med mænd, der aldrig havde haft sygdommen, mens andre ikke vidste, at de inkuberede kopper blandet med raske tropper. ‘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? Måske. 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. Hende 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 (27), 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) (611). 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.

Økologi

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.

Diskussion

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. I dag, 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.

Referencer

Figures
Tables

Please use the form below to submit correspondence to the authors or contact them at the following address:

John S. Marr, 6315 Pig Mountain Road, Free Union, VA 22940, USA

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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.

Denne artikel blev oprindeligt offentliggjort på 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


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