This question has been raised since the opening of Panama Canal (August 15, 1914).
It was known at that time that the biologic environment for Yellow
Fever propagation and maintenance appears to be favorable, A.aegypti is
widely distributed, and susceptible animal hosts, both man and monkey, are
abundant. There is no evidence that the people of India posses any racial
resistance to infection with yellow fever virus or unusual tolerance to the
disease. The rhesus monkey of India is one of the most susceptible of all the
primates and is much less tolerant to the disease than any of the African
monkeys.
Richards
in 1951 proposed the probable explanation of the absence of the disease in
India or elsewhere in the tropical Far East is that the virus was never
introduced. Formerly there were two overseas
routes that the virus might have taken in reaching India from Africa- the
more direct route from the east coast of Africa to India, and the longer route from the west coast around the Cape of Good Hope.
Though immunity surveys have revealed the existence of immunes in East African ports, the proportion of immunes is low. These low immunity rates imply
that the disease is infrequent and rarely,
if ever, reaches epidemic proportions.
Under such conditions the chances that the most direct route from East Africa
might convey the disease are not very great. It has been pointed out that
rather special conditions are
required for overseas transport, and the longer the voyage the less likely that
these conditions will be fulfilled. The voyage
from tropical West Africa to India is long, and in rounding the cape climatic conditions are frequently
encountered that are unfavorable to
the survival of the mosquito vector.
Theoretically, the risk of yellow fever in Asia is greater now than in the past
because of rapid modern transport, which can introduce viraemic persons or infected
mosquitoes in any of the receptive areas. Experimentally, A.aegypti mosquitoes collected in different places of Asia are able to transmit the virus to monkeys or newborn mice with variable
success, depending on their origin and the strain of virus utilized. This
conclusion has been extended to some other Asian mosquitoes such as A.pseudoscutellaris, A.polynesiensis and might be applicable
to A.albopictus (Bres, 1986). Today,
the possible reasons for its absence include both demographic and biologic factors.
Hypotheses include:
· Yellow Fever occurs in remote
areas and affects individuals engaged in subsistence farming, who are infrequent international travelers.
· Biologic factors that limit the risk of introduction include cross-protection, principally by dengue, against which nearly all
persons residing in Asia are immune.
· A third hypothesis is that A.aegypti strains in Asia have low vector competence for yellow fever
virus (Aitken et al., 1977).
It is
likely that all three mechanisms combine to reduce the likelihood of
introduction and spread of yellow fever virus in Asia (Monath, 2004).
Refrences:
- Richard M. Taylor (1951): Epidemiology. In: Strode G.K. (ed). Yellow Fever,McGraw Hill, N.Y.
- Bres, P.L.J. (1986): A century of progress in combating yellow fever.Bulletin of WHO. 64: (6), 775-786.
- Aitken T.H.G., Downs W.G., Shope R.E (1977): Aedes aegypti strain fitness for yellow fever transmission. Am.J.Trop.Med.Hyg.26: 985 – 989.
- Monath Thomas P. (2004): Yellow Fever Vaccine. Chapter 41. In Plotkin S.A. and Orienstein W.A. Vaccines 4th edition. Saunders
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