文档介绍：Medical Hypotheses 18: 51-52, 1985
CYSTIC FIBROSIS AND TRE PLAGW
W. F. Cassano, Fred Hutchinson Cancer Research Center
1124 Columbia St, Seattle, WA 98104
INTRODUCTION
In the study and practice of hematology, we are constantly remind-
ed of the influence the malaria parasite has had on the erythrocyte.
Modification of an erythrocyte surface protein (Duffy negative pheno-
type) to prevent parasite entry, and sickling hemoglobin to promote
rapid clearance of infected cells have been shown experimentally to
protect man from malaria infection (1,2,3). Other hemoglobinopathies,
glucose-&phosphate dehydrogenase deficiency, and thalassemia are also
circumstantially implicated in aborting the endoerythrocytic phase of
malaria (4). With this model in mind, and the knowledge that until
recently infectious diseases were the maior human predator, I would
suggest that cystic fibrosis, the most prevalent inherited disease of
people from northern European ancestry (5,6), is the result of an
adaptive response to Yersinia pestis epidemics.
BIOLOGY
Classic bubonic plague results from the transfer of zoonotic in-
fection in rodent populations to man by way of a flea vector. Proli-
feration of anism in draining lymph nodes (usually inguinal)
results in the formation of a bubo, septicemia, and death within 3-7
days. During the cold wet