Velike koze ubijajo staroselce - zgodovina

Velike koze ubijajo staroselce - zgodovina


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Kako so črne kozice uničile Azteke - in Španiji pomagale osvojiti ameriško civilizacijo pred 500 leti

Richard Gunderman ne dela za nobeno podjetje, organizacijo, ki bi imela koristi od tega člena, niti ne prejema lastniških deležev v njem in ne prejema sredstev, poleg tega pa ni razkril nobene ustrezne povezanosti, razen njihovega akademskega imenovanja.

Partnerji

Univerza Indiana financira kot članica The Conversation US.

Conversation UK od teh organizacij prejema sredstva

Nedavni izbruhi v ZDA so opozorili na nevarnost ošpic. Demokratična republika Kongo se bori proti smrtonosnemu izbruhu ebole, v katerem je umrlo na stotine ljudi.

Epidemije seveda niso nič novega. Nekatere razširjene nalezljive bolezni so močno spremenile potek človeške zgodovine.

Pred petsto leti, februarja 1519, je Španec Hernán Cortés odplul s Kube, da bi raziskal in koloniziral azteško civilizacijo v mehiški notranjosti. V samo dveh letih je bil asteški vladar Montezuma mrtev, glavno mesto Tenochtitlan je bilo zavzeto, Cortés pa je zahteval asteški imperij za Španijo. Špansko orožje in taktika sta imela vlogo, vendar so večino uničenja povzročile epidemije evropskih bolezni.


Zgodnja prizadevanja za nadzor

Ošpice so bile grozna bolezen. V povprečju so umrli 3 od 10 ljudi, ki so ga dobili. Ljudje, ki so preživeli, so imeli običajno brazgotine, ki so bile včasih hude.

Ena prvih metod za obvladovanje črnih koz je bila variolacija, proces poimenovan po virusu, ki povzroča črne koze (virus variole). Med variolacijo so bili ljudje, ki še nikoli niso imeli črnih koz, izpostavljeni materialu iz čirev črnih koz (pustul) s praskanjem materiala v roko ali vdihavanjem skozi nos. Po variolaciji so ljudje običajno razvili simptome, povezane z ošpicami, kot sta vročina in izpuščaj. Vendar pa je zaradi variacij umrlo manj ljudi, kot če bi naravne črne koze preboleli.

Osnova za cepljenje se je začela leta 1796, ko je angleški zdravnik Edward Jenner opazil, da so mlekarice, ki so zbolele za noricami, zaščitene pred črnimi kozami. Jenner je vedel tudi za varialne spremembe in ugibal je, da bi lahko izpostavljenost kravjim kozicam uporabili za zaščito pred črnimi kozami. Da bi preizkusil svojo teorijo, je dr. Jenner vzel material iz kravje norice na roki mlekarke Sarah Nelmes & rsquo in ga cepil v roko Jamesa Phippsa, 9-letnega sina vrtnarja Jenner & rsquos. Mesece kasneje je Jenner večkrat izpostavil Phippsa virusu variole, vendar Phipps ni nikoli razvil velikih koz. Sledilo je več poskusov in leta 1801 je Jenner objavil svojo razpravo & ldquoO izvoru cepljenja s cepivom. & Rdquo V tem delu je povzel svoja odkritja in izrazil upanje, da & ldquothe uničevanje črnih koz, najbolj strašne nadloge človeške vrste, mora biti končni rezultat te prakse. & rdquo

Cepljenje je postalo splošno sprejeto in postopoma nadomestilo prakso variolacije. V nekem trenutku v 19. stoletju se je virus, uporabljen za izdelavo cepiva proti črnim kozam, spremenil iz kravjih koz v virus vakcinije.

Na glavi 3000 let stare mumije faraona Ramzesa V. so našli sledi pustolov črnih koz, ki so jih objavile Svetovna zdravstvena organizacija (WHO)

Edward Jenner (1749 & ndash1823). Fotografija z dovoljenjem Nacionalne medicinske knjižnice.


Zmaga cepljenja

Človeški boj proti črnim kozam sega približno 2000 let. V Aziji je tehnika, znana kot variolacija, vključevala namerno okužbo osebe s pihanjem posušenih krast noric v nos. Tisti, ki so prejemali to zdravljenje, so zboleli za blago obliko bolezni, ki je razvila vseživljenjsko imuniteto.

Ključni preboj se je zgodil leta 1796, ko je poskus angleškega zdravnika Edwarda Jennerja pokazal, da bi lahko cepljenje z uporabo tesno povezanih kravjih koz zaščitilo pred črnimi kozami. Jennerjevo odkritje je utrlo pot kasnejšim programom cepljenja - še posebej ključnega pomena, ker ni učinkovitega zdravljenja za črne koze.

Leta 1967, ko je od 10 do 15 milijonov ljudi zbolelo za ošpicami, je Svetovna zdravstvena organizacija začela svetovno kampanjo izkoreninjenja, ki temelji na cepljenju. Postopoma je bila bolezen potisnjena nazaj na Afriški rog, zadnji znani naravni primer pa se je zgodil v Somaliji leta 1977.


Ali so zgodnji evropski raziskovalci domorodnim Američanom res dali odeje, okužene z noricami?

Na vprašanje: Ali so zgodnji evropski raziskovalci res dali domorodnim Američanom odeje, okužene z noricami?, Bi se večini ljudi zdelo smešno. Vendar pa morda še ni tako prikupljeno. O tem, ali se je to res zgodilo ali ne, je treba razpravljati, vendar obstaja dovolj dokazov, ki kažejo, da je bilo točno to dejanje mišljeno kot vojno orodje proti indijanskim domorodcem.

Zgodovina črnih koz
Prvi znani primer črnih koz se je zgodil leta 1507 na otoku Hispaniola. Ta otok je danes znan kot Haiti in Dominikanska republika. Mnogi verjamejo, da so španski raziskovalec Herman Cortes in 600 vojakov uporabili to bolezen, da bi leta 1520 premagali milijone Aztekov. Ošpice so se najverjetneje v Ameriko prebile prek romarjev, ki so pristali v Massachusettsu. Do sredine 18. stoletja so se črne koze razširile po vsej državi. Ker lahko bolezen dlje časa živi na tkanini ali v prahu, se je tako hitro razširila, da je zaslužna za izbris 30% vseh Indijancev, ki so se okužili. Morda so tudi črne koze igrale vlogo pri izumrtju Taina z Bahamov in Velikih Antilov.

Načrt črnih koz
Leta 1763 so se britanske sile med Pontiakovim uporom udeležile bitke s plemenom Ottawa. Po dokumentih, ki jih je odkril Peter d ’Errico, profesor pravnih študij na Univerzi v Massachusettsu v Amherstu, je Lord Jeffrey Amherst, poveljnik britanskih sil v Severni Ameriki, menda poslal pismo polkovniku Henryju Bouquetu. V tem pismu je očitno razpravljal o možnosti cepljenja Indijancev z noricami z odejami. To dejansko pismo je bilo kdaj odkrito, vendar je druga korespondenca med Amherstom in Bouquetom vsekakor kazala na obstoj takega pisma.

Ali je bil načrt izveden?
Odgovor na to vprašanje je, da nihče v resnici ne ve. Znano je, da je bilo to mogoče, saj so bile v Fort Pittu, kjer so nedavno odkrili bolezen, na voljo odeje. Drugi dejavnik, ki je naredil tako nori načrt izvedljiv, je bil Amherstov pogled na Indijance Indijance kot nekaj na ravni psa. Povedal je, da misli, da je zapravljanje teh ljudi (Ottawa) izguba dobrih ljudi, in je iskal načine, kako jih odpraviti, ne da bi tvegal življenja svojih mož. Omenil je celo kopiranje istih metod, ki so jih Španci uporabili za premagovanje Aztekov.

Kakšen je torej odgovor na vprašanje. Ali so zgodnji evropski raziskovalci domorodnim Američanom res dali odeje, okužene z noricami? Resnica ni znana, so pa posredni dokazi, ki zadostujejo za utemeljeno trditev. Britanski častnik je govoril o možnosti, da bi to dejansko storil, na voljo so bile odeje, zvijačna miselnost je bila na mestu in mnogi Indijanci so zaradi bolezni umrli. To je tako hudičevo pojmovanje, da se večini zdi nerazumljivo. A dejstvo ostaja, to so bili vojni časi in britanski vojaki so bili v vojni.


Prva različica: 1992

Churchill je leta 1992 objavil najzgodnejšo ponovitev svoje zgodbe o noricah, kot eno poglavje knjige, ki jo je uredila M. Annette Jaimes, ki je bila takrat Churchillova žena. Avtorstvo poglavja je bilo zapisano kot "Lenore A. Stiffarm with Phil Lane, Jr." Zdi se, da so resnični ljudje. Leta 2006 je kot del Churchillove obrambe pred obtožbami plagiatorstva trdil, da je to poglavje napisal duhov (Wesson et al, 2006, str. 40, fn. 78). Preiskovalni odbor Univerze v Koloradu za raziskovalno napako je sprejel Churchillovo trditev o pisanju duhov po nominalni vrednosti. Dejansko poglavje nosi Churchillove slogovne tike in ponovi izmišljene podrobnosti, ki bi jih Churchill še šestkrat objavil pod svojim imenom.

Vendar pa je tako izogibanje obtožbi plagiatorstva naredilo Churchilla ranljivega za nove obtožbe o izmišljotinah in ponarejanju v zvezi s svojo splošno pripovedjo o noricah. Poglavje "Stiffarm and Lane" (1992) trdi, da:

Vsekakor je bila distribucija odej, okuženih z noricami, ameriška vojska Mandanom v Fort Clarku na reki Missouri v današnji Južni Dakoti vzročni dejavnik pandemije 1836-1840. (str. 32)

Opomba "Stiffarm and Lane" se glasi:

Odeje so bile vzete iz ambulante ameriške vojske v St. Louisu in poslane navzgor na parniku St. Vojaško osebje jih je razdelilo 19. junija 1837. Glej Chardon, Francis A., Journal at Fort Clark, 1834-39, State Historical Society of South Dakota, Pierre, 1932. (str. 50, fn. 55)

Varno prikrit za lažnim naslovom, Churchill sproži ad hominem napad na Russella Thorntona, avtorja, katerega smrtnost ocenjuje, da se Churchill opira na svojo bajo o boginjah. Churchill pod krinko "Stiffarm and Lane" označuje Thorntona za "nekoliko zmedenega demografa Cherokeeja.", Ki je očitno zagledal priložnost za pridobitev "akademske verodostojnosti", tako da je zboru "uglednega" dodal težo svojega "domačega glasu" učenjakov [.] «(str. 27).


Bolezen za domorodne Američane še nikoli ni bila le bolezen

Ranljivost domačih skupnosti na epidemije ni zgodovinska nesreča, ampak neposredna posledica zatiralske politike in stalnega kolonializma.

O avtorju: Jeffrey Ostler je Beekmanov profesor zgodovine severozahoda in Pacifika na Univerzi v Oregonu. Je avtor Surviving Genocide: Native Nations in United States from the American Revolution to Bleeding Kansas.

Ker število umrlih zaradi COVID-19 narašča, so barvni ljudje očitno bolj ogroženi kot drugi. Med najbolj ranljivimi so Indijanci. Če želite razumeti, kako hude razmere COVID-19 postajajo za te skupnosti, razmislite o razmerah, ki se odvijajo za narod Navajo, ljudstvo z domovino v Arizoni, Novi Mehiki in Utahu. Med 170.000 prebivalci rezervata Navajo je bilo 23. aprila prijavljenih 1.360 okužb in 52 smrtnih primerov, stopnja umrljivosti 30 na 100.000. Le šest držav ima višjo cestnino na prebivalca.

Širjenje COVID-19 spominja na prejšnje izbruhe bolezni, ki so opustošili indijanske skupnosti. Mnogi od teh izbruhov so povzročili katastrofalno izgubo življenja, veliko večjo kot celo najslabši možni scenariji za COVID-19. Tudi pandemija gripe 1918–19, v kateri je umrlo približno 650.000 Američanov (0,6 odstotka od 106 milijonov prebivalcev leta 1920), je bleda v primerjavi z izgubami, ki so jih domorodni Američani utrpeli zaradi bolezni.

Do nedavnega so zgodovine bolezni in staroselci poudarjali »epidemije deviškega tla«. V skladu s to teorijo, popularizirano v Jared Diamond's Pištole, klice in jeklo, ko so Evropejci prispeli na zahodno poloblo, so prinesli bolezni (zlasti ošpice in črne koze), ki jih staroselci še nikoli niso doživeli. Teorija pravi, da zaradi teh bolezni niso imeli imunitete, je posledična epidemija vzela življenje 70 odstotkov ali več domorodcev po vsej Ameriki.

Nove raziskave pa ponujajo veliko bolj zapleteno sliko bolezni v zgodovini Američanov. Ta raziskava kaže, da epidemije deviškega tal niso bile tako pogoste, kot so prej mislile, in se osredotoča na to, kako so bolezni v desetletjih in stoletjih večkrat napadale domorodne skupnosti po Prvi so prišli Evropejci. Bolezni po stiku so hromile ne toliko zato, ker avtohtonim prebivalcem primanjkuje imunitete, ampak zato, ker so pogoji, ki sta jih ustvarila evropski in ameriški kolonializem, domorodne skupnosti naredili ranljive. Hipoteza o deviških tleh in epidemiji je bila dragocena v nasprotju s prejšnjimi teorijami, ki so pripisovale upadanje prebivalstva Indijancev rasni manjvrednosti, vendar je njen edinstven poudarek na bioloških razlikah pomenil, da so kolapsi prebivalstva le zgodovinske nesreče. Nova štipendija s poudarkom na pomenu družbenih razmer, ki jih ustvarjajo človeške odločitve in dejanja, daje veliko bolj motečo sliko. Prav tako nam pomaga razumeti težave, s katerimi se danes spopadajo domorodne skupnosti, ko se borijo proti novemu koronavirusu.

Nedvomno je prišlo do epidemije deviških tal. Leta 1633 je na primer epidemija noric prizadela domorodne skupnosti v Novi Angliji, kar je zmanjšalo populacijo Mohegan in Pequot s skupaj 16.000 na samo 3.000. Epidemija se je razširila na Haudenosaunee v New Yorku, vendar ne bolj zahodno od tega. Norice so doletele skupnosti v dolini Ohio in Velikih jezerih šele leta 1756–57, stoletje ali več po prvem stiku z Evropejci. Ko se je to zgodilo, je bilo zato, ker so domorodni borci, ki so bili v sedemletni vojni novačeni v boj za Francoze proti Britancem, na vzhodu okužili virus in okužili njihove skupnosti, ko so se vrnili domov. Pomanjkanje imunitete je bilo pomembno, vendar so motnje, ki so nastale zaradi vojne, spodbudile širjenje koz.

Norice so na jugovzhod prispele šele leta 1696, stoletje in pol po odpravi Hernando de Soto. Nekoč je veljalo, da de Sotovi možje prenašajo črne koze, vendar je to stališče odražalo napačno domnevo, da so Evropejci vedno okuženi z ošpicami in vedno nalezljivi. De Sotova ekspedicija je sicer povzročila izbruh bolezni v domorodnih skupnostih, vendar je bil razlog v tem, da je nasilno vojskovanje odprave pripeljalo do izbruhov patogenov, kot je griža, ki je že bila prisotna v Ameriki. Ko so črne koze končno prišle na jugovzhod, so se hitro razširile iz Virginije v vzhodni Teksas po omrežjih, ki jih je ustvarila angleška trgovina z domačimi ujetniki za zasužnjevanje v njihovih obalnih in zahodnoindijskih kolonijah. Napadi, zajemanje in prevoz človeških teles so ustvarili poti za virus črnih koz. Še huje, vojna in njeni spremljevalci so že oslabili ta telesa - podhranjenost, izpostavljenost in pomanjkanje paliativne oskrbe.

Do konca 18. stoletja je bila večina domorodnih skupnosti v tistih, ki bodo sčasoma postale Združene države, izpostavljena črnim kozam. Kljub temu, da so se osi v 19. stoletju ponavljale, njen vpliv ni bil povezan s pomanjkanjem predhodne izpostavljenosti, ampak s prisotnostjo neugodnih družbenih razmer. Zaradi teh istih pogojev bi lahko bile domorodne skupnosti dovzetne za številne druge bolezni, vključno s kolero, tifusom, malarijo, grižo, tuberkulozo, skrofulo in alkoholizmom. Domača ranljivost ni imela - in nima - nič opraviti z rasno manjvrednostjo ali pa, od teh prvih incidentov, prej s pomanjkanjem imunitete, ampak ima vse opraviti s konkretnimi politikami, ki jih vodijo vlada ZDA, njene države in njeni državljani.

Razmislite o vplivu indijskega zakona o odstranitvi. Uradno sprejeta leta 1830 je ta politika zahtevala premestitev domorodcev vzhodno od reke Mississippi na "indijsko ozemlje" (kar bo sčasoma postalo Oklahoma in Kansas). Skoraj vsi so slišali za Cherokee Trail of Tears, vendar le redko velja za zdravstveno krizo, ki jo povzroča ZDA. Izgon Cherokeeja iz domovine v Gruziji, Severni Karolini in Tennesseeju je imel tri faze. V prvem je ameriška vojska prisilno izselila čeroke iz njihovih domov in jih več mesecev zadržala v koncentracijskih taboriščih z neustreznim zavetjem, nezadostno hrano in brez vira čiste vode. Tabori so postali pasti smrti. Od 16.000 ljudi, ki so jih držali, jih je približno 2000 umrlo zaradi griže, oslovskega kašlja, ošpic in "vročine" (verjetno malarije). V drugi fazi potovanja proti zahodu je umrlo dodatnih 1500, saj so ljudje, ki so že bili bolni in še oslabljeni zaradi podhranjenosti, travme in izpostavljenosti, podlegli številnim patogenom. V mesecih po doseganju Oklahome - tretji fazi - je dodatnih 500 umrlo zaradi podobnih vzrokov. Število žrtev je bilo 4.000 ali 25 odstotkov od prvotnih 16.000, ki so jih prisilili iz svojih domov.

Čeprav je pot solz Cherokee najbolj znana, je bilo na desetine drugih takšnih prisilnih odstranitev. Creeks, Seminoles, Chickasaws, Choctaws, Senecas, Wyandots, Potawatomis, Sauks and Mesquakies, Ojibwes, Ottawas, Miamis, Kickapoos, Poncas, Modocs, Kalapuyas in Takelmas predstavljajo le delni seznam narodov, ki so utrpeli sledi solz. Niso vsi doživeli enake smrtnosti kot Cherokee, vendar so mnogi doživeli, za nekatere pa je bilo cestnina še višja. Zavezniška Sauksa in Mesquakiesa sta se morala štirikrat preseliti iz svojih vasi v zahodnem Illinoisu - enkrat v osrednjo Iowo, enkrat v zahodno Iowo, enkrat v Kansas in nazadnje v Oklahomo. Leta 1832, v času prvega izgona, je Sauks in Mesquakies štelo 6.000. Do leta 1869, ko so jih končno poslali v Oklahomo, jih je bilo le 900, kar je neverjetna izguba 85 odstotkov. Leto za letom so neusmiljene bolezni, vključno z izbruhom črnih koz, leta 1851, vzele veliko življenj. Nizka rodnost in umrljivost dojenčkov, ki sta posledica podhranjenosti, bolezni in travm, sta ovirala zamenjavo prebivalstva. Katastrofa Sauk in Mesquakie ni bila nesreča. To je bila neposredna in predvidljiva posledica odločitev, ki so jih sprejele Združene države in njihovi državljani, da so domorodce odstranili iz zaželenih dežel in jih potisnili drugam.

Navajo (Dinés, kot se sami imenujejo v svojem jeziku) so bili izseljeni tudi iz svojih domovin. Pozimi 1863–64 je ameriška vojska sledila taktiki požgane zemlje-uničila je breskve in koruzna polja-, da bi jih odpeljala v pusto rezervacijo v Bosque Redondo, na reki Pecos v Novi Mehiki. Na 250-miljskem prisilnem pohodu, znanem kot Dolgi sprehod, je na poti umrlo več sto od 8.000 do 9.000 Dinéjev. V naslednjih štirih letih je Dinés zaradi bolezni in lakote izgubil kar 2500 ljudi. V svoji najtemnejši uri pa so voditelji Dinéja uspešno premagali vladne uradnike, da so jih izpustili iz zapora in se vrnili domov. A čeprav se je njihovo prebivalstvo sčasoma povečalo, ostajajo zapuščine Dolge poti. Zgodovinarka Dinéja Jennifer Denetdale ugotavlja, da "huda revščina, zasvojenost, samomor in kriminal v rezervatih imajo vse svoje korenine v Dolgem sprehodu."

Ko so se konec marca v rezervatu Navajo začeli pojavljati primeri COVID-19, je predsednik plemena Jonathan Nez na svojem Facebooku govoril s svojimi ljudmi. Ob sklicevanju spominov na Dolgi sprehod je »pozval občane, naj si med seboj pomagajo,« jih je spomnil, »takrat je od mnogih naših prednikov prišlo najboljše, si pomagali, nosili breme za starejše, nosili otroke za naše matere. " "Zdaj smo na vrsti," je dejal, "da razmišljamo o svoji prihodnosti, svojih otrocih, vnukih." Zaradi stalnega kolonializma je boj proti COVID-19 izziv. Čeprav so Navajo suverena država z lastnimi viri, imajo Dinés visoko incidenco stanj - sladkorno bolezen, hipertenzijo in pljučne bolezni - ki povečujejo njihovo dovzetnost za hudo bolezen zaradi koronavirusa. Pomanjkanje dostopa do čiste vode otežuje umivanje rok. Mnogi si ne morejo privoščiti hrane, sredstev za razkuževanje rok in drugih potrebščin. In akutno primanjkuje bolniških postelj in zdravstvenega osebja.

Mnogi javni uslužbenci, zdravstveni strokovnjaki in novinarji opozarjajo na nesorazmeren vpliv COVID-19 na barvne skupnosti. Kljub temu so veliki segmenti Amerike ravnodušni, če ne celo sovražni do priznavanja teh razlik in neenakosti, na katerih temeljijo. Indijanci so širši javnosti veliko bolj vidni kot športne maskote kot kot dejanske skupnosti. Trumpova administracija se je sprva uprla zagotavljanju kakršne koli olajšave plemenskim narodom v paketu spodbud v višini 2 bilijona dolarjev, sprejetem v začetku aprila, in čeprav je zakonodaja na koncu namenila 10 milijard dolarjev plemenskim vladam, jih ministrstvo za finance, ki je bilo zadolženo za razdeljevanje teh sredstev, ni uspelo izplačati. Po besedah ​​senatorja Nove Mehike Toma Udalla uradniki ministrstva za finance "ne vedo, kako na primeren način komunicirati s plemeni in preprosto ne opravijo dela."

Boj proti nevidnosti domorodcev seveda pomeni večjo ozaveščenost o tem, kako COVID-19 vpliva nanje, in okrepljena prizadevanja za zagotovitev sredstev za boj proti sedanjemu izbruhu. Pomeni tudi globlje razumevanje zgodovine ameriških Indijancev in bolezni. Čeprav je bila hipoteza o devstveni zemlji in epidemiji deviško zemljo morda dobronamerna, se osredotoča na kratek, čeprav grozljiv trenutek prvega stika, bolezen varno pošlje v daljno preteklost in kolonizatorjem zagotovi alibi. Avtohtone skupnosti se borijo bolj kot virus. Spopadajo se s stalno dediščino stoletja nasilja in odvzema lastništva.


Epidemija velikih koz

Elizabeth A. Fenn preučuje malo znano katastrofo, ki je preoblikovala zgodovino celine.

Na križarjenju po severozahodni obali Amerike leta 1792 je bil kapitan George Vancouver v težavah. Kje so se spraševali, kje so bili vsi domačini? Dežela je bila v izobilju, z navidez neomejeno ponudbo lososa in sladke vode, vendar je bilo ljudi presenetljivo malo. Namesto tega je britanski navigator našel zapuščene vasi. Prvi, ki so ga naleteli južno od otoka Vancouver na obali zaliva Discovery, je bil "prenatrpan s plevelom, med katerim je bilo najdenih več človeških lobanj in drugih kosti, razpršeno razpršenih naokoli".

Ko je Vancouver začrtal ožino Juan de Fuca, se je prizor redno ponavljal. "Med to odpravo" je zapisal član posadke Thomas Manby, "med njimi smo videli ogromno zapuščenih vasi. sposobni zadržati več sto prebivalcev. Za Manbyja je bil zaključek neizbežen: "V nekem primeru je bila ta država precej izseljena, toda iz kakšnega vzroka je težko ugotoviti." Vancouver se je strinjal. Verjel je, da vsi dokazi kažejo, da "ta država ni bila v nobenem zelo oddaljenem obdobju veliko bolj naseljena kot zdaj".

Res je prišlo do katastrofe, ki je bila tako velika, da njene priče in žrtve niso mogle ceniti njenega obsega. V letih od 1775 do 1782, ko je revolucionarna vojna preoblikovala družbo in politiko vzdolž vzhodne obale, je povsem drugačna kataklizma pretresla celotno severnoameriško celino. Velika in strašna kataklizma je bila črne koze.

Povzroča ga zmerno nalezljiv virus, znan kot Variola major , so se prvi znaki črnih koz pojavili dvanajst dni po izpostavitvi, običajno z okužbo dihal. Sprva blagi so bili zgodnji simptomi podobni simptomom gripe. Vključevali so glavobol, bolečine v hrbtu, zvišano telesno temperaturo, bruhanje in splošno slabo počutje. V mnogih primerih so se žrtve počutile bolje že po prvih dneh ali dveh, pogosto misleč, da so res trpele zaradi gripe.

Olajšanje pa je bilo minljivo. Četrti dan se je obraz zardel in pojavile so se prve boleče lezije - ne na površini kože, ampak v ustih, grlu in nosnih poteh. V štiriindvajsetih urah se je pojavil značilen kožni izpuščaj. Pri nekaterih se je izpuščaj obrnil navznoter, krvavil pod kožo in skozi sluznico. Ti bolniki so prezgodaj umrli zaradi krvavitve iz oči, nosu, dlesni ali nožnice. Pri večini bolnikov pa so se pustule potisnile na površino kože. Če ne bi nastopili skupaj, je bila napoved precej ugodna. Če pa so pustule naletele drug na drugega pri tako imenovanih "konfluentnih" črnih kozah, so imeli bolniki vsaj 60 -odstotno možnost, da umrejo.

Ko je izpuščaj napredoval v ustih in grlu, je postalo pitje oteženo in pogosto je prišlo do dehidracije. Okoli desetega dne, ko so se pustule zmehčale in postale mehurčki, je veliko dehidriranih bolnikov preprosto absorbiralo tekočino, ki so jo vsebovali. Kmalu zatem so po besedah ​​bostonskega zdravnika iz osemnajstega stoletja rane "začele teči in vonjati". Tudi v higienskih razmerah se lahko pojavijo sekundarne bakterijske okužbe s posledicami, ki so v celoti tako hude kot posledice ošpic. Proti koncu drugega tedna so se začele tvoriti kraste. William Bradford je v svojem opisu črnih koz med Indijanci iz Narragansetta leta 1634 opisal to stanje:

. ko lulajo na svojih trdih podlogah, poxe se lomijo in delajo pomembne stvari in se raztezajo druga v drugo, njihova koža se razcepi (zaradi tega) na podloge, na katere se poležejo, ko jih obrnejo, bo celo stran zbežalo naenkrat [f].

V tretjem tednu je umrljivost močno upadla. Vročina je popustila in bolniki so se na splošno izboljšali, saj so grde brazgotine nadomestile kraste in pustule. Običajen potek bolezni, od začetka do izgube vseh krast, je trajal približno en mesec. Preživeli so bili blagoslovljeni, čeprav so pogosto imeli brazgotine in v redkih primerih celo zaslepljeni zaradi bolezni. Ko so nekoč preboleli ošpice, so bili zdaj imuni. Nikoli več ne bi zboleli za boleznijo.

Čeprav je bilo strah, Američani iz osemnajstega stoletja niso imeli neoboroženih črnih koz. Tudi brez razumevanja virologije so uporabili dve orožji proti bolezni: izolacijo in inokulacijo. Izolacija ali karantena sta preprosto pomenili izogibanje stiku med bolniki s to boleznijo in posamezniki, ki so dovzetni za to. Posteljnina in oblačila so lahko predmet posebnega ravnanja. Pravilno opravljena karantena lahko pogosto ustavi nadaljnjo okužbo. V kolonialnem obdobju so izolacijo uporabljali tako kolonisti kot staroselci.

Drugo orožje - uporabljeno tudi po odkritju cepljenja Edwarda Jennerja leta 1796 - je bilo cepljenje. Za razliko od cepljenja, pri katerem je bil uporabljen virus kravjih koz, je pri inokulaciji prišlo do namerne okužbe občutljivega posameznika z virusom Variola, običajno z zarezo na roki. Zaradi razlogov, ki se znanstvenikom izmikajo vse do danes, je bila cepljena črna koza v večini primerov veliko manj virulentna kot "naravna" oblika bolezni. Preživeli so si pridobili vseživljenjsko imuniteto, prav tako kot "naravne" črne koze, vendar je bila smrtnost občutno nižja.

Prišlo pa je do ulova: posamezniki, ki so bili cepljeni, so vseeno zboleli za črnimi kozami, zato so bili popolnoma sposobni okužiti druge z boleznijo. Če se ne izvaja v strogi karanteni, je operacija verjetno sprožila epidemijo kot jo ustavila. Zaradi tega je bilo cepljenje v angleških kolonijah zelo kontroverzno, kjer so bili izbruhi črnih koz osrednje redki. V Angliji pa je bila bolezen že dolgo endemična in postopek je dosegel širšo sprejemljivost. Ti združeni dejavniki so pomenili, da so britanske sile v zgodnjih fazah ameriške revolucije veliko bolj verjetno kot Američani pridobile imuniteto proti Variola virus.

Od zgodnjega španskega raziskovanja je prišlo do uničujočih izbruhov črnih koz, vendar nobenega ni mogoče tako natančno dokumentirati, kot je epidemija, iz katere je Vancouver zagledal mračne ostanke. Prvi znaki so se pojavili med zgodnjimi konflikti ameriške revolucije 1775-76. V treh različnih epizodah - obleganju Bostona, obleganju Quebeca in mobilizaciji Dunmorejevega etiopskega polka - so se norice dvignile. Na koncu sta ti epizodi, zlasti prvi dve, prisilili generala Georgea Washingtona in njegovo zdravstveno osebje k pomembnim političnim odločitvam v zvezi z nadzorom proti črnim kozam v celinski vojski.

Do leta 1775 so bile opravljene predpriprave. Zakon o sladkorju, Zakon o žigu, Čajanka, Bostonski pokol - vsak je prispeval k vse večjemu razkolu med kolonijami in matično državo. Z vsakim novim dejanjem so se sklicali sestanki, zbrala se je množica in glasniki so tekali naprej in nazaj med kolonijami. Zgodovinske metafore, ki opisujejo, da so se kolonisti "okužili" s "okužbo svobode", se zdijo primerne: pogoji so bili res popolni za dejansko okužbo.

Epidemične črne koze so se najprej pojavile v Bostonu, v žarišču revolucionarne gorečnosti. V okoliških mestih so se leta 1774 zgodili osamljeni incidenti, a januarja 1775 se je bolezen uveljavila v samem Bostonu.

Prva vojna bitka se je zgodila aprila, bolezen pa je cvetela poleti, medtem ko se je celinska vojska okopala po mestu. Da bi preprečili, da bi med svojimi četami zasedla, so Američani ustanovili namensko bolnišnico proti črnim kozam v svežem ribniku blizu Cambridgea. 4. julija 1775 je Washington ukazal:

Nobena oseba ne sme iti v ribnik s sladko vodo na ribolov ali ob kateri koli drugi priložnosti, saj obstaja nevarnost, da bi črne kozice vnesli v vojsko.

Vsak vojak, ki kaže "najmanj simptomov malih noric", se je soočal s takojšnjo karanteno.

Prizadevanja za nadzor so bila uspešna vse poletje. Toda novembra, ko so se Bostonci obračali v zaprtih prostorih, da bi se ubranili zimske mrzlice, je med njimi narasla bolezen. Hkrati sta se morala Washington in njegovi možje spopasti z znatnim begom beguncev iz prizadetega mesta. "General Howe je 300 prebivalcem Bostona ukazal, da v slabih pogojih pridejo v Point Shirley," je Washington pisal kongresu. 'JAZ . Strašno me je strah, da so sporočali o noricah, saj je to v Bostonu veliko. Beguncem je prepovedal vstop v ameriško taborišče.

Nato so v prvem tednu decembra prispeli štirje britanski dezerterji z zastrašujočo novico. Njihov poveljnik, general William Howe, so trdili, da je namerno okužil ubežnike "z namenom širjenja malih boginj med četami". Sprva je Washington govoricam pripisal malo zaslug. Ko pa so med razseljenimi Bostonci izbruhnile ošpice, so bili Američani prisiljeni podvojiti svoja prizadevanja pri obvladovanju črnih koz.

Ta prizadevanja so se obrestovala. Bolezen se je med ameriškimi silami razširila šele potem, ko so se Britanci umaknili 17. marca 1776. Nato so se po obleganju ljudje zlili v Boston. "Boston", je zapisal Moses Morse, "je postal bolnišnica z noricami". Vrhunec epidemije je bil julija.

Obupani, da bi obvladali širjenje, so se mestni izbrani ljudje odločno odločili: čeprav je bilo cepljenje v Bostonu tradicionalno prepovedano, so se julija za dvanajst dni odpovedali prepovedi. Izbrani možje so postavili stražnike po mestu. Nihče ne more vstopiti, nihče z vidnimi simptomi ne more zapustiti. Nazadnje je sredi septembra epidemija izgorela.

Tako dobrih novic z drugih front ni bilo. 6. maja 1776 je po bednem petmesečnem obleganju kanadskega mesta Quebec več kot 1500 Američanov pobegnilo navzgor po reki St Lawrence, ko se je 900 britanskih rednih turistov izkrcalo, da bi razbremenili kvebeško posadko. Med obleganjem so se morali Američani spopadati tako z Britanci kot z črnimi kozami. Medtem ko je karantena delovala v Bostonu, od začetka v Quebecu ni uspela. 1. maja 1776, pet dni pred umikom, je 900 od 1.900 ameriških vojakov pred Quebecom zbolelo, predvsem zaradi velikih koz.

Ko se je 6. maja začel kaotičen umik, je celo videz karantene izginil: moški, ki so se z velikimi črnimi kozami borili s snegom do kolen, skupaj z moškimi, ki nikoli niso imeli te bolezni, drugi pa se niso zavedali, da se okužijo z ošpicami, pomešanimi z zdravimi četami. ‘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? Mogoče. 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. Ona 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.

Ekologija

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.

Diskusija

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. Danes, 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.

Reference

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.

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


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