Rõuged tapavad põlisameeriklasi - ajalugu

Rõuged tapavad põlisameeriklasi - ajalugu


We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.


Kui rõuged laastasid asteegid - ja aitasid Hispaanial 500 aastat tagasi vallutada Ameerika tsivilisatsiooni

Richard Gunderman ei tööta, ei konsulteeri, ei oma aktsiaid ega saa rahastust ühestki ettevõttest või organisatsioonist, kes sellest artiklist kasu saaks, ning pole avaldanud ühtegi olulist seost peale nende akadeemilise ametisse nimetamise.

Partnerid

Indiana ülikool rahastab The Conversation USA liikmena.

Conversation UK saab nendelt organisatsioonidelt rahastust

Hiljutised haiguspuhangud USA -s on juhtinud tähelepanu leetrite ohtudele. Kongo Demokraatlik Vabariik võitleb surmava Ebola puhanguga, mis on tapnud sadu inimesi.

Epideemiad pole muidugi midagi uut. Ja mõned laialt levinud nakkushaigused on inimkonna ajaloo kulgu põhjalikult muutnud.

Viissada aastat tagasi, 1519. aasta veebruaris, asus hispaanlane Hernán Cortés Kuubalt teele, et uurida ja koloniseerida asteekide tsivilisatsiooni Mehhiko sisemaal. Vaid kahe aasta jooksul oli asteekide valitseja Montezuma surnud, pealinn Tenochtitlan vallutati ja Cortés oli Hispaaniale nõudnud asteekide impeeriumi. Oma osa oli Hispaania relvastusel ja taktikal, kuid suurema osa hävingust põhjustasid Euroopa haiguste epideemiad.


Varajase kontrolli jõupingutused

Rõuged olid kohutav haigus. Keskmiselt suri kolm inimest igast kümnest, kes selle sai. Ellujäänud inimestel olid tavaliselt armid, mis olid mõnikord rasked.

Üks esimesi meetodeid rõugete tõrjeks oli variolatsioon - protsess, mis sai nime rõugeid põhjustava viiruse (variola viirus) järgi. Variolatsiooni ajal puutusid inimesed, kellel ei olnud kunagi rõugeid, rõugehaavade (pustulite) materjali, kriimustades materjali käe sisse või hingates sisse nina kaudu. Pärast variolatsiooni tekkisid inimestel tavaliselt rõugetega seotud sümptomid, nagu palavik ja lööve. Variolatsiooni tagajärjel suri aga vähem inimesi kui siis, kui nad oleksid rõuged looduslikult omandanud.

Vaktsineerimise alus sai alguse 1796. aastal, kui inglise arst Edward Jenner märkas, et lehmapiimad saanud piimamehed on rõugete eest kaitstud. Jenner teadis ka variolatsioonist ja arvas, et kokkupuudet lehma rõugetega saab kasutada rõugete eest kaitsmiseks. Oma teooria proovilepanemiseks võttis dr Jenner materjali lehmapiimavalu käest piimamehe Sarah Nelmes & rsquo käest ja inokuleeris selle Jenneri ja rsquose aedniku 9-aastase poja James Phippsi käsivarrele. Kuud hiljem paljastas Jenner Phippsi mitu korda variola viirusega, kuid Phippsil ei tekkinud kunagi rõugeid. Järgnesid veel katsed ja 1801. aastal avaldas Jenner oma traktaadi & ldquo vaktsiiniinokulatsiooni päritolu kohta. olla selle praktika lõpptulemus. & rdquo

Vaktsineerimine sai laialdaselt tunnustatud ja asendas järk -järgult variolatsiooni. Mingil hetkel 1800 -ndatel muutus rõugevaktsiini valmistamiseks kasutatav viirus lehma rõugest vaktsiiniaviiruseks.

Vaarao Ramses V 3000-aastase muumia peast leiti rõugepustulite jälgi. Foto viisakalt Maailma Terviseorganisatsiooni (WHO) poolt

Edward Jenner (1749 ja ndash1823). Foto viisakalt Rahvusraamatukogu.


Vaktsineerimise võit

Inimeste võitlus rõugete vastu pärineb umbes 2000 aastat. Aasias hõlmas variolatsioonina tuntud tehnika teadlikult inimese nakatamist, puhudes kuivatatud rõugete koorikuid ninna. Need, kes said seda ravi, said kerge haiguse vormi, arendades eluaegset immuunsust.

Oluline läbimurre tehti aastal 1796, kui inglise arsti Edward Jenneri katse näitas, et inokuleerimine, kasutades lähedalt seotud lehma rõugeid, võib kaitsta rõugete eest. Jenneri avastus sillutas teed hilisematele vaktsineerimisprogrammidele - eriti oluline, kuna rõugete tõhus ravi puudub.

1967. aastal, mil umbes 10–15 miljonit inimest haigestusid rõugetesse, alustas Maailma Terviseorganisatsioon vaktsineerimisel põhinevat ülemaailmset likvideerimiskampaaniat. Järk -järgult tõrjuti haigus Aafrika Sarvele tagasi ja viimane teadaolev loodusjuhtum leidis aset Somaalias 1977. aastal.


Kas varajased Euroopa maadeavastajad andsid tõepoolest põlisameeriklastele rõugete tekke?

Kui küsida küsimus, kas varajased Euroopa maadeavastajad tõepoolest andsid põlisameeriklastele rõugetega nakatatud tekid ?, leiaks enamik inimesi, et küsimus on naeruväärne. Siiski ei pruugi see nii kaugele tuua. Seda, kas see tegelikult juhtus või mitte, avatakse aruteludeks, kuid on piisavalt tõendeid selle kohta, et täpset tegu peeti sõjavahendiks põliselanike indiaanlaste vastu.

Rõugete ajalugu
Esimene teadaolev rõugejuhtum leidis aset 1507. aastal Hispaniola saarel. Seda saart tuntakse täna Haiti ja Dominikaani Vabariigina. Paljud usuvad, et see oli Hispaania maadeavastaja Herman Cortes ja 600 sõdurit, kes kasutasid haigust miljonite asteekide võitmiseks aastal 1520. Rõuged jõudsid tõenäoliselt Ameerikasse Massachusettsi maabunud palverändurite kaudu. 18. sajandi keskpaigaks olid rõuged levinud üle kogu riigi. Kuna haigus võib pikka aega elada riidel või tolmus, levis see nii kiiresti, et selle põhjuseks on 30% nakatunud indiaanlaste hävitamisest. Rõuged võisid samuti kaasa aidata Bahama saarte ja Suur -Antillide Taino väljasuremisele.

Rõugeplaan
Aastal 1763 asusid Briti väed Pontiac ’s mässu ajal lahingusse Ottawa hõimuga. Amherstis Massachusettsi ülikooli õigusteaduse professori Peter d ’Errico avastatud dokumentide kohaselt saatis Põhja -Ameerika Briti vägede ülem Lord Jeffrey Amherst väidetavalt kolonel Henry Bouquet'le kirja. Selles kirjas arutas ta ilmselt võimalust indiaanlasi rõugetesse tekke kasutades inokuleerida. See tegelik kiri on kunagi avastatud, kuid muu kirjavahetus Amhersti ja Bouquet'i vahel näitas kindlasti sellise kirja olemasolu.

Kas plaan täideti?
Vastus sellele küsimusele on see, et keegi tegelikult ei tea. On teada, et see oli võimalik, kuna Fort Pittis oli olemas tekid, kus haigus hiljuti avastati. Teine tegur, mis nii hullumeelse plaani teoks teeb, oli Amhersti vaade Ameerika põliselanikule kui koera tasemele. Ta oli märkinud, et tema arvates on heade meeste raiskamine nende loomade (Ottawa) jälitamiseks ja otsis võimalusi nende kõrvaldamiseks ilma oma meeste eluga riskimata. Ta viitas isegi samade meetodite kopeerimisele, mida hispaanlased olid asteekide võitmiseks kasutanud.

Niisiis, milline on vastus küsimusele. Kas varajased Euroopa maadeavastajad andsid Ameerika põliselanikele tõepoolest rõugetega nakatunud tekid? Tõde on teadmata, kuid need on kaudsed tõendid, mis on piisavalt põhjendatud. Briti ohvitser rääkis võimalusest seda tegelikult teha, tekid olid saadaval, kelmikas mõtteviis oli paigas ja paljud indiaanlased surid haigusesse. See on nii kuratlik arusaam, et enamik inimesi peab seda arusaamatuks. Kuid fakt jääb faktiks, need olid sõjaajad ja Briti sõdurid sõdisid.


Esimene versioon: 1992

Churchill avaldas 1992. aastal oma rõugete tekijuttude varaseima teadaoleva iteratsiooni kui ühe peatüki raamatust, mille toimetas M. Annette Jaimes, kes oli sel ajal Churchilli naine. Peatüki autoriks oli aga "Lenore A. Stiffarm koos Phil Lane, Jr." Nad näivad olevat tõelised inimesed. 2006. aastal väitis ta osana Churchilli kaitsest plagiaadisüüdistuste vastu, et on selle peatüki kummituslikult kirjutanud (Wesson jt, 2006, lk 40, jn 78). Colorado Ülikooli uurimiskomitee uurimiste väärkäitumise kohta võttis Churchilli kummituskirjutamisnõude vastu nimiväärtuses. Tõepoolest, peatükk kannab Churchilli stiilitikke ja kordab väljamõeldud detaile, mida Churchill hakkaks oma nime all uuesti avaldama veel kuus korda.

Plagiaadisüüdistusest kõrvalehoidmine muutis aga Churchilli haavatavaks uute rõivaste tekitatud narratiivi valmistamise ja võltsimise eest. Peatükk "Stiffarm and Lane" (1992) väidab, et:

Kindlasti oli Ameerika Ühendriikide armee poolt rõugetega nakatunud tekkide jagamine Mandansile Fort Clarkis, Missouri jõe ääres tänapäeva Lõuna-Dakotas, põhjustanud 1836–1840 pandeemiat. (lk 32)

"Stiffarm ja Lane" lõppmärkus on järgmine:

Tekid võeti USA armee haiglast St. Louis'is ja saadeti aurulaevaga St. Neid jagasid armee töötajad 19. juunil 1837. Vt Chardon, Francis A., Journal of Fort Clark, 1834-39, State Dorota State Society of South Dakota, Pierre, 1932. (lk 50, viide 55)

Turvaliselt varjatud joonise taha peidetud Churchill alustab ad hominem rünnakut Russell Thorntoni vastu, autor, kelle suremuse hinnangul Churchill tugineb oma rõugete tekilugule. "Stiffarmi ja Lane'i" varjus nimetab Churchill Thorntoni kui "pisut segaduses tšerokide demograafi. Kes näib olevat näinud võimalust omandada" akadeemiline usaldusväärsus ", lisades oma" emakeelse hääle "kaalu lugupidamisele teadlaste [.] "(lk 27).


Haigus pole põliselanike jaoks kunagi olnud lihtsalt haigus

Põliskogukondade haavatavus epideemiate suhtes ei ole ajalooline õnnetus, vaid rõhuva poliitika ja jätkuva kolonialismi otsene tulemus.

Autorist: Jeffrey Ostler on Oregoni ülikooli Loode- ja Vaikse ookeani ajaloo Beekmani professor. Tema on autor Ellujäänud genotsiid: põlisrahvad ja Ameerika Ühendriigid Ameerika revolutsioonist kuni Kansase verejooksuni.

Kuna COVID-19 hukkunute arv on suurenenud, on värvilistel inimestel selgelt suurem risk kui teistel. Kõige haavatavamate hulka kuuluvad indiaanlased. Mõistmaks, kui kohutavaks COVID-19 olukord nende kogukondade jaoks muutub, kaaluge olukorda, mis areneb Navajo rahvusel, rahval, kelle kodumaa on Arizonas, New Mehhikos ja Utahis. 23. aprilli seisuga oli Navajo Reservationi 170 000 inimese seas teatatud 1360 nakkusest ja 52 surmast, suremus oli 30 juhtu 100 000 kohta. Vaid kuues osariigis on maksumäär inimese kohta kõrgem.

COVID-19 levik tuletab meelde varasemaid haiguspuhanguid, mis on laastanud põliselanike kogukondi. Paljud neist haiguspuhangutest põhjustasid katastroofilisi inimkaotusi, mis on palju suuremad kui isegi COVID-19 halvimad stsenaariumid. Isegi 1918–1919 gripipandeemia, milles hukkus hinnanguliselt 650 000 ameeriklast (0,6 protsenti 1920. aasta 106 miljoni elanikkonnast), kahvatub võrreldes põliselanike haigusest kannatanud kahjudega.

Kuni viimase ajani on haiguste ja põlisameeriklaste ajalugu rõhutanud „neitsi mulla epideemiaid”. Selle teooria kohaselt on see populaarne Jared Diamondis Relvad, mikroobid ja teras, kui eurooplased läänepoolkerale saabusid, tõid nad kaasa haigused (eriti leetrid ja rõuged), mida põlisrahvas polnud kunagi kogenud. Kuna neil puudus nende haiguste suhtes immuunsus, siis teooria kohaselt võtsid sellest tulenevad epideemiad kogu Ameerikas 70 % või rohkem põliselanike elu.

Uued uuringud annavad aga Ameerika India ajaloos haigustest palju keerulisema pildi. See uuring näitab, et neitsimulla epideemiad ei olnud nii tavalised, kui varem arvati, ning suunavad tähelepanu sellele, kuidas haigused aastakümnetel ja sajanditel korduvalt põliselanikke ründasid pärast Eurooplased saabusid esimest korda. Kontaktijärgsed haigused olid halvavad mitte niivõrd seetõttu, et põlisrahvastel puudus immuunsus, vaid seetõttu, et Euroopa ja USA kolonialismi loodud tingimused muutsid põliskogukonnad haavatavaks. Neitsi-mulla-epideemia hüpotees oli väärtuslik varasemate teooriate vastu, mis omistasid Ameerika põliselanike arvu vähenemise rassilisele alaväärsusele, kuid selle ainulaadne rõhutamine bioloogilisele erinevusele tähendas, et elanikkonna kokkuvarisemine oli midagi muud kui ajaloolised õnnetused. Rõhutades inimeste otsuste ja tegudega loodud sotsiaalsete tingimuste tähtsust, annab uus stipendium palju häirivama pildi. Samuti aitab see mõista probleeme, millega põliskogukonnad täna uue koroonaviiruse vastu võitlevad.

Kahtlemata esines neitsi-mulla epideemiaid. Näiteks aastal 1633 tabas Uus -Inglismaa põliselanike kogukondi rõugeepideemia, mis vähendas Mohegani ja Pequoti populatsioone kokku 16 000 -lt vaid 3000 -le. Epideemia levis New Yorgi Haudenosaunee'i, kuid mitte kaugemale sellest läände. Rõuged tabasid Ohio oru ja Suurte järvede kogukondi alles aastatel 1756–57, sajand või rohkem pärast esmast kontakti eurooplastega. Kui see juhtus, oli see tingitud sellest, et seitsmeaastase sõja ajal prantslaste eest brittide vastu võitlemiseks värvatud põliselanike võitlejad olid idas viiruse saanud ja koju naastes nende kogukonnad nakatanud. Immuunsuse puudumine oli oluline, kuid just sõja tagajärjel tekkinud katkestused soodustasid rõugete levikut.

Rõuged jõudsid kagusse alles 1696. aastal, poolteist sajandit pärast Hernando de Soto ekspeditsiooni. Kunagi arvati, et de Soto mehed kannavad rõugeid, kuid see vaade peegeldas ekslikku eeldust, et eurooplased on alati rõugetega nakatunud ja alati nakkavad. De Soto ekspeditsioon põhjustas põliselanike kogukondades haigusi, kuid põhjus oli selles, et ekspeditsiooni vägivaldne sõda tõi kaasa selliste haigustekitajate puhangud nagu düsenteeria, mis oli Ameerikas juba olemas. Kui rõuged lõpuks Kagu -piirkonda tabasid, levis see kiiresti Virginiast Ida -Texasesse võrgustike kaudu, mille lõi Inglise kaubandus põliselanikega orjastamiseks nende ranniku- ja Lääne -India kolooniates. Inimeste kehade rüüstamine, hõivamine ja transportimine lõi teed rõugeviirusele. Asja tegi veelgi hullemaks see, et sõjad ja nende kaaslased - alatoitumus, kokkupuude ja palliatiivse ravi puudumine - nõrgestasid neid asutusi.

18. sajandi lõpuks oli enamik põliskogukondi, kes lõpuks muutusid Ameerika Ühendriikideks, olnud rõugetega kokku puutunud. Sellegipoolest, kui rõuged kordusid 19. sajandil, ei korreleerunud selle mõju mitte eelneva kokkupuute puudumisega, vaid ebasoodsate sotsiaalsete tingimustega. Need samad tingimused muudaksid põliskogukonnad vastuvõtlikuks paljude teiste haiguste, sealhulgas koolera, tüüfuse, malaaria, düsenteeria, tuberkuloosi, skrofula ja alkoholismi suhtes. Looduslikul haavatavusel ei olnud ega ole mingit pistmist rassilise alaväärsusega või pärast neid esialgseid juhtumeid pigem puutumatuse puudumisega, on see kõik seotud Ameerika Ühendriikide valitsuse, selle osariikide ja kodanike konkreetse poliitikaga.

Mõelge India kolimisseaduse mõjule. See poliitika, mis võeti ametlikult vastu 1830. aastal, nõudis põlisrahvaste ümberpaigutamist Mississippi jõest ida pool „India territooriumile” (millest saavad lõpuks Oklahoma ja Kansas). Peaaegu kõik on kuulnud Cherokee pisaraterajast, kuid seda peetakse harva USA põhjustatud tervisekriisiks. Cherokee väljasaatmine oma kodumaalt Gruusias, Põhja -Carolinas ja Tennessees toimus kolmes etapis. Esimesena tõstis USA armee tšerokid sunniviisiliselt kodudest välja ja hoidis neid mitu kuud koonduslaagrites, kus oli ebapiisav peavarju, ebapiisav toit ja puhas vesi. Laagritest said surmapüüdjad. Neist peetud 16 000 inimesest suri umbes 2000 düsenteeria, läkaköha, leetrite ja “palaviku” (tõenäoliselt malaaria) tõttu. Teises faasis, teekonnas läände, hukkus veel 1500 inimest, kuna inimesed, kes olid juba haiged ja alatoitumise, traumade ja kokkupuute tõttu veelgi nõrgemad, alistusid mitmele patogeenile. Kuudel pärast Oklahomasse jõudmist - kolmandas faasis - suri sarnastel põhjustel veel 500 inimest. Hukkunuid oli 4000 ehk 25 protsenti esialgsest 16 000 -st, kes sunniti kodudest minema.

Kuigi Cherokee pisarate rada on kõige tuntum, oli selliseid sunniviisilisi eemaldamisi veel kümneid. Creeks, Seminoles, Chickasaws, Choctaws, Senecas, Wyandots, Potawatomis, Sauks and Mesquakies, Ojibwes, Ottawas, Miamis, Kickapoos, Poncas, Modocs, Kalapuyas ja Takelmas esindavad vaid osalist loetelu rahvastest, kes kannatasid pisaraid. Mitte kõik ei kogenud sama suremust kui Cherokee, kuid paljud kogesid ja mõne jaoks oli teemaks veelgi suurem. Liitlased Saukid ja Mesquakies olid sunnitud neli korda oma Illinoisi lääneosa küladest kolima - üks kord Iowa kesklinna, kord Iowa lääneosa, üks kord Kansasesse ja lõpuks Oklahomasse. 1832. aastal, esimese väljasaatmise ajal, oli sauke ja mesquakies 6000. Aastaks 1869, kui nad lõpuks Oklahomasse saadeti, oli nende elanikkond vaid 900, mis oli jahmatav 85 protsenti. Aasta -aastalt võtsid järeleandmatud haigused, sealhulgas rõugete puhang 1851. aastal, palju elusid. Madal viljakus ja imikute suremus, mis on tingitud alatoitumisest, haigustest ja traumadest, takistas elanikkonna asendamist. Sauki ja Mesquakie katastroof ei olnud õnnetus. See oli otsene ja ettenähtav tagajärg Ameerika Ühendriikide ja selle kodanike otsustele, mille kohaselt põliselanikud soovitavatelt maadelt ära võeti ja kuhugi mujale suruti.

Navajosid (diinid, nagu nad oma keeles viitavad iseenesele) aeti välja ka kodumaalt. Talvel 1863–64 järgis USA armee kõrbenud maa taktikat-hävitas nende virsikupuud ja maisipõllud-, et viia need New Mexico osariigis Pecos jõe äärde Bosque Redondos asuvasse viljatu reservatsiooni. 250 miili pikkusel sunnitud marsil, mida tuntakse pika jalutuskäiguna, hukkus teel 8000 kuni 9000 Dinés mitusada. Järgmise nelja aasta jooksul kaotas Dinés haiguste ja nälja tõttu koguni 2500 inimest. Kuid kõige pimedamal ajal võitsid Diné juhid edukalt valitsusametnikke, et nad vabastataks vanglast ja naaseksid koju. Kuid kuigi nende elanikkond on aja jooksul kasvanud, jäävad Pika jalutuskäigu pärandid alles. Diné ajaloolane Jennifer Denetdale märgib, et „tõsise vaesuse, sõltuvuse, enesetappude ja kuritegude reservatsioonide juured on pikal jalutuskäigul”.

Kui märtsi lõpus hakkas Navajo reservatsioonis ilmnema COVID-19 juhtumeid, rääkis hõimu president Jonathan Nez oma inimestega Facebookis. Pika jalutuskäigu mälestusi kokku kutsudes kutsus ta „kodanikke üksteist aitama”, tuletades neile meelde, „just siis tulid paljud meie esivanematest välja parimad, aidates üksteist välja, kandes vanematele koormat, kandes lapsi meie jaoks. emad. ” "Nüüd on meie kord," ütles ta, "mõelda oma tulevikule, oma lastele, lastelastele." Pidev kolonialism muudab COVID-19 vastu võitlemise väljakutseks. Kuigi navahod on suveräänne rahvas, kellel on oma ressursid, on Dinésel palju selliseid haigusi - diabeet, hüpertensioon ja kopsuhaigus -, mis suurendavad nende vastuvõtlikkust koroonaviirusest raskelt haigestuda. Puhtale veele juurdepääsu puudumine raskendab käte pesemist. Paljud inimesed ei saa endale lubada toitu, käte desinfitseerimisvahendeid ega muud vajalikku. Ja haiglavooditest ja meditsiinitöötajatest on terav puudus.

Paljud riigiametnikud, terviseeksperdid ja ajakirjanikud juhivad tähelepanu COVID-19 ebaproportsionaalsele mõjule värvikogukondadele. Sellegipoolest on Ameerika suured segmendid nende erinevuste ja nende aluseks oleva ebavõrdsuse tunnustamisel ükskõiksed, kui mitte lausa vaenulikud. Ameerika põliselanikud on laiemale avalikkusele nähtavad palju sagedamini kui spordimaskotid kui tegelikud kogukonnad. Trumpi administratsioon oli esialgu vastu sellele, et aprilli alguses vastu võetud 2 triljoni dollari suuruses stimuleerimispaketis hõimurahvastele igasugust leevendust ei pakuta ja kuigi seadusandlus eraldas hõimuvalitsustele lõpuks 10 miljardit dollarit, ei ole rahandusministeerium, kelle ülesandeks on need vahendid jaotada, neid välja maksta. New Mexico senaatori Tom Udalli sõnul ei tea rahandusministeeriumi ametnikud „hõimudega sobival viisil suhelda ja nad lihtsalt ei saa tööd tehtud.”

Põlisrahvaste nähtamatuse vastu võitlemine tähendab muidugi suuremat teadlikkust sellest, kuidas COVID-19 neid mõjutab, ja suuremaid jõupingutusi ressursside pakkumiseks, mis aitavad neil praeguse puhanguga võidelda. See tähendab ka sügavama arusaamise loomist Ameerika indiaanlaste ja haiguste ajaloost. Ehkki neitsi-mulla-epideemia hüpotees võis olla hästi kavatsetud, saadab selle keskendumine põgusale, kui kohutavale esmase kontakti hetkele haigused ohutult kaugesse minevikku ja annab kolonisaatoritele alibi. Põlisrahvaste kogukonnad võitlevad rohkem kui viirus. Nad võitlevad sajanditepikkuse vägivalla ja vallutamise jätkuva pärandiga.


Suur rõugeepideemia

Elizabeth A. Fenn uurib vähetuntud katastroofi, mis muutis mandri ajalugu.

Kapten George Vancouver oli 1792. aastal Ameerika looderannikul rännates hädas. Kuhu jäid ta, kas kõik pärismaalased olid? Maa oli külluslik, pealtnäha piiramatu lõhe- ja mageveevaru, kuid inimesi oli silmatorkavalt vähe. Selle asemel leidis Briti navigaator mahajäetud külad. Esimene, mis avastati Vancouveri saarest lõuna pool Discovery lahe kaldal, oli „umbrohust üleküllastunud, mille hulgast leiti mitu inimkolju ja muid luid, mis olid laiali hajutatud”.

Kui Vancouver kaardistas Juan de Fuca väina, kordus stseen regulaarselt. "Selle ekspeditsiooni ajal" märkis meeskonnaliige Thomas Manby: "nägime väga palju mahajäetud külasid, mõned neist. suudab majutada sadu elanikke. ” Manby jaoks oli järeldus vältimatu: „Mingil juhul on see riik oluliselt tühjenenud, kuid mis põhjusel, on raske kindlaks teha.” Vancouver nõustus. Tema arvates näitasid kõik tõendid, et „mitte ühelgi väga kaugel perioodil pole see riik olnud palju rahvaarvuga kui praegu”.

Õnnetus oli tõesti nii suur, et isegi selle tunnistajad ja ohvrid ei osanud selle ulatust hinnata. Aastail 1775–1782, kui vabadussõda muutis ühiskonda ja poliitikat idarannikul, raputas kogu Põhja -Ameerika mandrit väga erinev kataklüsm. Kataklüsm, tohutu ja kohutav, oli rõuged.

Põhjuseks mõõdukalt nakkav viirus, mida tuntakse Variola major , esmased rõugete tunnused tekkisid kaksteist päeva pärast kokkupuudet, tavaliselt hingamisteede infektsiooni kaudu. Alguses olid kerged sümptomid sarnased gripiga. Nende hulka kuulusid peavalu, seljavalu, palavik, oksendamine ja üldine halb enesetunne. Paljudel juhtudel hakkasid ohvrid pärast esimest või kahte päeva end paremini tundma, arvates sageli, et nad on tõepoolest grippi põdenud.

Leevendus oli aga üürike. Neljandaks päevaks nägu õhetas ja ilmnesid esimesed valusad kahjustused - mitte naha pinnal, vaid suus, kurgus ja ninakanalites. Kahekümne nelja tunni jooksul tekkis iseloomulik nahalööve. Mõnel pöördus lööve sissepoole, veritses naha all ja limaskestade kaudu. Need patsiendid surid varakult, veritsesid silmadest, ninast, igemetest või tupest. Enamikul patsientidest surusid pustulid aga naha pinnale. Kui nad kokku ei jooksnud, oli prognoos üsna hea. Kuid kui pustulid jooksid üksteisega kokku nn konfluentsete rõugete korral, oli patsientidel vähemalt 60 % tõenäosus surra.

Kui lööve progresseerus suus ja kurgus, muutus joomine keeruliseks ja sageli tekkis dehüdratsioon. Umbes kümnendal päeval, kui pustulid pehmendasid ja muutusid villiliseks, imendusid paljud dehüdreerunud patsiendid lihtsalt neis sisalduva vedeliku tagasi. Varsti pärast seda, kaheksateistkümnenda sajandi Bostoni arsti sõnade kohaselt, hakkasid haavandid "jooksma ja lõhnama". Isegi hügieenitingimustes võivad tekkida sekundaarsed bakteriaalsed infektsioonid, mille tagajärjed on sama tõsised kui rõugete. Teise nädala lõpus hakkasid tekkima koorikud. William Bradford kirjeldas 1634. aastal Narragansetti indiaanlaste rõugete kirjelduses seda seisundit:

. nad leelistavad oma kõvadel mattidel, pintsel puruneb ja on oluline ning jooksevad üksteise otsa, nahk lõheneb (põhjustel) matte, mille külge nad leekides lehvivad, pöörleb terve külg korraga [f].

Kolmandal nädalal langes suremus järsult. Palavik vaibus ja patsiendid üldiselt paranesid, kui ebameeldivad armid asendasid kärnad ja pustulid. Tavaline haiguse kulg, alates esialgsest algusest kuni kõigi kärnade kadumiseni, võttis aega umbes ühe kuu. Ellujääjaid, kuigi sageli armistusid ja harvadel juhtudel isegi haigusest pimestatud, õnnistati. Olles kord rõugeid talunud, olid nad nüüd immuunsed. Nad ei haaraks seda haigust enam kunagi.

Kuigi see oli hirmutav, ei seisnud XVIII sajandi ameeriklased relvastamata rõugetega silmitsi. Isegi ilma viroloogiast aru saamata kasutasid nad haiguse vastu kahte relva: isolatsiooni ja inokuleerimist. Isoleerimine või karantiin tähendas lihtsalt kokkupuute vältimist haigete ja sellele vastuvõtlike inimeste vahel. Voodipesu ja riideid võidakse eriliselt käsitleda. Nõuetekohase toimimise korral võib karantiin sageli edasise nakatumise peatada. Koloniaalajal kasutasid isolatsiooni nii kolonistid kui ka põliselanikud.

Teine relv, mida kasutati isegi pärast seda, kui Edward Jenner avastas vaktsineerimise 1796. aastal, oli inokuleerimine. Erinevalt vaktsineerimisest, milles kasutati lehma rõugeviirust, hõlmas inokuleerimine vastuvõtliku isiku tahtlikku nakatumist Variola viirusega, tavaliselt käe sisselõike kaudu. Põhjustel, mis teadlastest tänaseni hoiduvad, oli inokuleeritud rõuged enamikul juhtudel palju vähem virulentsed kui haiguse loomulik vorm. Ellujääjad võitsid eluaegse immuunsuse, nagu ka loomulike rõugete korral, kuid suremus oli märgatavalt väiksem.

Siiski oli üks konks: inokuleeritud isikud said küll rõugeid ja seetõttu olid nad täielikult võimelised teisi haigusega nakatama. Kui seda ei teostata range karantiini all, käivitas operatsioon sama tõenäoliselt epideemia kui ka peatas selle. Sel põhjusel oli inokulatsioon Inglise kolooniates, kus rõugepuhangud olid suhteliselt haruldased, väga vastuoluline. Inglismaal oli haigus aga juba ammu endeemiline ja protseduur saavutas laiema heakskiidu. Need kombineeritud tegurid tähendasid, et Ameerika revolutsiooni varases staadiumis said Briti väed ameeriklastest tunduvalt tõenäolisemalt immuunsuse. Variola viirus.

Hispaania varajase uurimise ajal oli olnud laastavaid rõugepuhanguid, kuid ühtegi neist ei saa nii täielikult dokumenteerida kui epideemiat, mille Vancouver oli näinud süngeid jäänuseid. Esimesed märgid ilmnesid Ameerika revolutsiooni esimestel konfliktidel aastatel 1775-76. Kolmes erinevas episoodis - Bostoni piiramine, Quebeci piiramine ja Dunmore'i Etioopia rügemendi mobiliseerimine - tõstis rõuge pea üles. Lõpuks sundisid need episoodid, eriti kaks esimest, kindral George Washingtoni ja tema meditsiinitöötajaid tegema olulisi poliitilisi otsuseid, mis puudutavad rõugete tõrjet kontinentaalses armees.

1775. aastaks olid eelvõistlused tehtud. Suhkruseadus, templiseadus, teeõhtu, Bostoni veresaun - kumbki oli aidanud kaasa kolooniate ja emamaa vahelisele kasvavale lõhele. Iga uue tegevusega kogunesid koosolekud, kogunesid rahvahulgad ja sõnumitoojad kihutasid kolooniate vahel edasi -tagasi. Ajaloolised metafoorid, mis kirjeldavad kolonistide nakatumist „vabaduse levikuga”, tunduvad seega sobivad: tingimused olid tõelise nakkuse jaoks tõepoolest ideaalsed.

Epideemilised rõuged tulid esmakordselt esile Bostonis, see oli revolutsioonilise tulihingeline kasvukoht. Üksikuid vahejuhtumeid oli ümberkaudsetes linnades esinenud 1774. aastal, kuid 1775. aasta jaanuariks oli haigus Bostonis endas võimust võtnud.

Sõja esimene lahing toimus aprillis ja haigus levis kogu suve, samal ajal kui mandriarmee oli kinnistunud linna ümber. Vältimaks, et see oma vägede seas võimust võtaks, rajasid ameeriklased Cambridge'i lähedal Fresh Pondis spetsiaalse rõugehaigla. 4. juulil 1775 andis Washington käsu:

Ükski inimene ei tohi minna magevee tiiki kala püüdma ega mõnel muul juhul, kuna võib tekkida oht, et väikseid rõugeid tuuakse sõjaväkke.

Iga sõdur, kellel ilmnesid vähimad rõugete sümptomid, seisis kohe karantiini all.

Püüded kontrolli saavutada olid kogu suve edukad. Kuid novembris, kui bostonlased pöördusid siseruumidesse talvise jaheduse tõrjumiseks, tõusis haigus nende seas. Samal ajal pidid Washington ja tema mehed leppima märkimisväärse põgenike väljarändamisega kannatada saanud linnast. "Kindral Howe on käskinud 300 Bostoni elanikku viletsas seisus Point Shirley'sse," kirjutas Washington Kongressile. 'Mina. kardan kohutavalt, et nad suhtlevad rõugetega, kuna see on levinud Bostonis. ” Ta keelas põgenikud Ameerika laagrist.

Siis saabusid detsembri esimesel nädalal neli Briti deserterit hirmutavate uudistega. Nende väejuht kindral William Howe oli väidetavalt põgenikke tahtlikult nakatanud, eesmärgiga levitada väikseid rõugeid vägede vahel. Algul andis Washington kuulujutule vähe au. Kuid kui ümberasustatud bostonlaste seas puhkesid rõuged, olid ameeriklased sunnitud rõugete tõrjeks oma jõupingutusi kahekordistama.

Need pingutused tasusid end ära. Haigus levis Ameerika vägede seas alles pärast seda, kui britid taganesid 17. märtsil 1776. Siis tungisid inimesed piiramisjärgselt Bostonisse. "Boston", kirjutas Moses Morse, "on muutunud haiguseks koos rõugetega". Epideemia saavutas haripunkti juulis.

Olles meeleheitel leviku ohjeldamiseks, tegid linna valikulised mehed dramaatilise otsuse: ehkki inokuleerimine oli Bostonis traditsiooniliselt keelatud, loobusid nad keelust juulis kaheteistkümneks päevaks. Valitud mehed postitasid valvureid üle linna. Keegi vastuvõtlik ei saanud siseneda ja nähtavate sümptomitega keegi ei saanud sealt lahkuda. Lõpuks, septembri keskel põles epideemia end läbi.

Teistelt rindelt selliseid häid uudiseid ei tulnud. 6. mail 1776 põgenesid pärast viletsat viiekuulist Kanada linna Quebeci piiramist üle 1500 ameeriklase St Lawrence'i jõe äärest, kui 900 Briti püsiklienti lahkusid Quebeci garnisoni leevendamiseks. Piiramise ajal pidid ameeriklased võitlema nii brittide kui ka rõugetega. Kuigi karantiin oli Bostonis töötanud, ebaõnnestus see Quebecis algusest peale. 1. mail 1776, viis päeva enne taganemist, oli 900 Quebeci eel olnud Ameerika sõjaväelasest 900 haige, peamiselt rõugetega.

Kui 6. mail algas kaootiline tagasitõmbumine, kadus isegi välimus karantiinist: rõugete käes vaevlevad mehed võitlesid põlvedeni ulatuva lume kõrval nende inimestega, kellel polnud seda haigust kunagi olnud, teised aga ei teadnud, et nad hauduvad rõugeid, mis on segatud tervete vägedega. ‘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? Võib -olla. 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. Tema 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.

Ökoloogia

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.

Arutelu

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. Täna, 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.

Viited

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

Comment submitted successfully, thank you for your feedback.


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