does not provide any scientific or medical data to support this statement. Honigbaum agrees with Curtin and Humphreys, as he states that Europeans saw Africans as a suitable labor force due to these real or perceived immunities. He also argues that the slave trade was responsible for the endemic nature of malaria and yellow fever in the Caribbean. Honigsbaum additionally delves into geopolitical ramifications of disease and credits the devastating influence of malaria and yellow fever on effectively hampering British intentions in the Caribbean towards Spanish holdings. Thus, Honigsbaum’s opinion agrees with the general consensus of the scholars examined in this essay, in that Africans brought to the Americas were perceived by Europeans
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Webb posits that African slaves and European settlers bringing the parasite in their bodies and in stowaway Anopheles, combined with the presence of an indigenous population, provided the sufficient mix of parasite, vector, and human population density to allow for malaria to take root. The turning point, he argues, was the Portuguese establishment of sugar plantations in the mid sixteenth century in Brazil, the earliest use of African slave labor in the Americas. The plantation model spread, and thus malaria spread though South and Central America and to the Greater Caribbean. Webb states in British North America, malaria’s foothold began in Jamestown. This contradicts Margaret Humphreys' opinion. Humphreys does agree that vivax likely manifested in Jamestown, but places falciparum’s arrival in the 1680s in South Carolina. Both use credible sources. Enslaved Africans carrying the Duffy mutation were immune to the lesser strain of vivax malaria already present in the Americas from European transmission. Webb states that “most” Africans arriving in Brazil carried a “functional” resistance to the more deadly falciparum strain. It is unclear if he refers to the Sickle Cell mutation or to some other claim of inherited resistance. He also states that enslaved Africans and their descendants may have some inherited immunity to the yellow fever virus. He bases this opinion on Kiple. Thus, Webb appears to align with the previous author’s discussed in this paper in that the perception that there is a racial component to malaria and/or yellow fever and
Webb posits that African slaves and European settlers bringing the parasite in their bodies and in stowaway Anopheles, combined with the presence of an indigenous population, provided the sufficient mix of parasite, vector, and human population density to allow for malaria to take root. The turning point, he argues, was the Portuguese establishment of sugar plantations in the mid sixteenth century in Brazil, the earliest use of African slave labor in the Americas. The plantation model spread, and thus malaria spread though South and Central America and to the Greater Caribbean. Webb states in British North America, malaria’s foothold began in Jamestown. This contradicts Margaret Humphreys' opinion. Humphreys does agree that vivax likely manifested in Jamestown, but places falciparum’s arrival in the 1680s in South Carolina. Both use credible sources. Enslaved Africans carrying the Duffy mutation were immune to the lesser strain of vivax malaria already present in the Americas from European transmission. Webb states that “most” Africans arriving in Brazil carried a “functional” resistance to the more deadly falciparum strain. It is unclear if he refers to the Sickle Cell mutation or to some other claim of inherited resistance. He also states that enslaved Africans and their descendants may have some inherited immunity to the yellow fever virus. He bases this opinion on Kiple. Thus, Webb appears to align with the previous author’s discussed in this paper in that the perception that there is a racial component to malaria and/or yellow fever and