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ISSN: 2329-891X
Journal of Tropical Diseases & Public Health
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New Natural Anti-Malaria Source in India: A Brief Communication

Ariel Kushmaro1, Tamara Awerbuch-Friedlander2*and Richard Levins2

1Department of Biotechnology Engineering, Faculty of Engineering Sciences, Ben Gurion University, Beer Sheba 84105, Israel

2Department of Population and International Health Harvard School of Public Health, 665 Huntington Avenue, Boston, Massachusetts 02115, USA

*Corresponding Author:
Tamara Awerbuch-Friedlander
Department of Global Health and Population
Harvard School of Public Health
665 Huntington Ave, Boston, MA 02115, USA
Tel: 617- 432 – 2505
E-mail: [email protected]

Received Date: October 21, 2015 Accepted Date: November 13, 2015 Published Date: November 20, 2015

Citation: Kushmaro A, Friedlander TA, Levins R (2015) Temperature Effects on the Basic Reproductive Number (R0) Of West Nile Virus, Based On Ecological Parameters: Endemic Vs. New Emergence Regions. J Trop Dis 4:187. doi:10.4172/2329-891X.1000187

Copyright: © 2015 Kushmaro A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Eco-epidemiology; West Nile Virus; Basic reproductive number; Global warming


West Nile virus (WNV), an arbovirus of the genus Flavivirus and the family Flaviviridae, was first recognized in 1937 after its isolation from a native of Uganda [1]. It is transmitted to hosts mainly by mosquitoes of the genera Culex; although Aedes, and others have been also involved in selected geographic locations [2,3]. Already in the 1950s birds were identified as the main reservoirs of WNV in the Nile delta [4,5] and later confirmed in other part of the world [6-8]. In the USA, birds such as geese, pigeons, crows, blue jays and house sparrows were found to be infected with WNV 7. It has been suggested that robins may serve as a primary amplifying host of the virus, and develop a high-level of viremia that lasts for several days [9]. During the viremia period, adult female mosquitoes may get infected via a blood meal they take, and pass the infection to not yet infected birds. Thus, the infection circulates in nature in an enzootic cycle within bird reservoirs; humans and other mammals are affected mainly as dead-end hosts as they do not contribute to the amplification of the virus [10-12].

Epidemiology and ecology

In 1994 to 1999, WNV emerged in temperate regions of Europe, North Africa and North America, presenting a threat to public health, as well as equine and avian health [8,12]. Although about 80% of people infected with WNV are asymptomatic, and only about 1% progress to severe disease, some might seriously be affected with neurological complications or death [13,14]. Outbreaks were reported in Algeria in 1994, Romania 1996-1997, the Czech Republic in 1997, the Democratic Republic of Congo in 1998, Russia in 1999, and the USA in 1999 [6,14-18]. During 1999-2006, the WNV extended its range throughout the new world and is expected to continue to expand [3,10,19-21]. Migratory birds are thought to participate in the geographical spread of the virus in North America [6,22].

However the virus, affecting humans and circulating within avian reservoirs was already recognized in the middle of last century. The first outbreak of the virus in Israel and Egypt occurred in the 1950s [4,5,23]. In 1980, an outbreak was reported in southern Israel [24,25] followed by a major outbreak in the year 2000 [26-28]. The main mosquito vectors in Israel and Egypt are Culex perexiguus [29-31] and C. pipiens [4,32]. Typically wild birds are the principal reservoir of the West Nile virus. The virus has been isolated from a number of wetland and terrestrial avian species including migratory birds such as the barred warbler, turtledove, pigeons, wagtails, geese and white storks [31,33]. Some of these birds play an important role in intercontinental transmission [34]. This may be due to sufficiently prolonged viremia as was documented in several bird species. Such prolonged viremia is likely to occur during migration because of its substantial physiologicstress on birds. Outbreaks of the virus occur during late summer or early fall, coinciding with the arrival of large concentrations of migratory birds and with elevated mosquito population. Indeed, WNV was isolated from migrating white storks that landed in Eilat, Israel in 1998 [33]; the flock migrated southward for the first time and had not previously flown over Israel. It was suggested that the storks became infected in Europe prior to the time of migration [33]. It is also likely that the virus is carried by the migration of birds in the spring, from Africa to European breeding grounds via Israel as a transit and restingplace [35]. Supporting the hypothesis that migratory birds play a role in the geographic spread of the virus, the finding that WNV isolated from Culex perexiguus caught along the Kenya-Uganda border in the spring of 1998, demonstrated a high similarity with a Culex pipiens mosquito isolate from Romania in 1996 [36]. Although migratory birds are considered an important factor in the geographic spread of WNV and its introduction in new geographic locations, most probably the domestic ones are those involved in its amplification cycle [4,5].

Endemic vs. New-emergence regions

The seminal study of Work et al (1955) on WNV from the Nile Delta, developed the concept of non-endemic, transitional and endemic zones. It was argued that differences in the various environmental components among these zones accounted for differences in the persistence of the virus. In this paper, we use the Basic Reproduction Number, R0, derived from a formula based on ecological properties of the various components of thetransmission cycle, to compare the risk of WNV in Israel which emerged in the 1950s, thus considered an endemic region, to that of North America, where the virus emerged in 1999, thus considered a new-emergent region [10,14]. The assumption is that similar mosquito species are involved in the two regions and they also share an almost genetically identical viral strains, suggesting that the infection in the US may have originated in Israel [37]. Recent work demonstrated that the virus in North America has been evolving and is now more efficient at disseminating through a mosquito [38].

The hypothesis is that the progression of the epidemic in these two zones will differ according to their sensitivity to environmental components as captured by the equation of the Basic Reproductive Number, R0, defined as the expected number of infected birds originated by one infected bird in the population, presented in Figure 1.


Figure 1: Dry whole Ayurvedic punica, chloroplast stage (juvenile); thick dermis; yields the highest anti-malaria drug moieties. Native product of Indian sub-continent, suited well to indo agro-meteorology.

Thus, we use R0 to compare the vulnerability of these two zones as a function of temperature, as there are yearly variations and because of predictions of systematic global warming. In addition, it is anticipated that climate changes associated with global warming will have an effect particularly on vector-borne diseases such as WNV [39] and their spread to new zones [40]. Such a direct effect of elevated temperature on WNV has already been seen in parts of Russia and Israel [41].

The Basic reproductive number, R0

It has been observed experimentally that WNV transmission depends on entomological factors related to the interaction of mosquitoes with its reservoir and also to the level of immunity of this reservoir [42]. The high level of complexity involved in WNV spread is captured by the basic reproductive number, R0 (Figure 1).

In the process of elucidating the role of mosquitoes in the transmission of malaria, Ross constructed the first mathematical model for describing epidemics [43]. Ross’s model was expanded by Macdonald (1957) and by other researchers to model other vector-borne diseases [44]. One of the basic results of the analysis of the Ross-Macdonald model is the derivation of the basic reproductive number R0 for malaria in terms of entomological parameters related to mosquitoes. R0 is the number of secondary cases arising from a single case in a susceptible population, and depends on ecological variables [45], one of which is the duration of the infectious period within the reservoir (“see equation in Figure 1”) [46]. Once the infection agent is introduced R0>1, the disease will propagate. When R0<1, the infection cannot be sustained. In the case of malaria, for which the concept was originally developed, humans are not only severely affected hosts but also reservoirs and participants in the infection cycle. However, the concept of R0 was later used to explore the potential for the rise and fall of other infectious diseases with different modes of transmission and non-human reservoir [47]. Recently, R0 was specifically derived for WNV from a system of nine ordinary differential equations model that linked bird-reservoirs with mosquito-vectors and human hosts. Although humans were included in the model, a qualitative analysis of the equations system rendered the result, that for a certain threshold of R0, depending on parameters related only to the mosquito-bird cycle, its value could be less than a unit and, thus in principle, WNV could be eradicated [48].

Materials and Methods

In our work, we use the original definition of R0 as presented in Figure 1 focusing only on the bird-mosquito cycle, which is relevant for virus amplification. The annotated equation Figure 1 includes definitions of the ecological parameters and their dependence on environmental factors.

Calculations for R0 as a function of temperature in endemic region (e.g., Israel and Egypt) vs. new emergence region (e.g., North America) are based on various parameter estimates from the literature and presented in Table 1 [4,5,34,49-53]. The entomological parameters pertain to species of the genera Culex and Aedes, which are the main species involved in WNV transmission. The probability that an infected mosquito will transmit the infection (b1) is 0.9 for both locations in temperatures between 23 to 35°C, 0.4 at 20°C 0.3 at 18°C and 0.8 at 22°C [50,51,54-57]. However, the probability that an infected bird will transmit the infection (b2) is a lot higher in new emergence region since WNV is rather new and most of the birds are susceptible to the virus and will develop high viremia. In endemic area the majority of the birds are likely to be resistant and non-infectious [4,58]. It is more likely that juvenile birds that have not yet been exposed to the virus will be more susceptible to infection and, therefore, more infections and become an important component of the WNV amplification cycle [4,59]. Thus, we chose as a preliminary estimate: b2=0.2 in endemic region and b2=0.8 in new emergence region. These estimates are based on the work of Work et al (1955), showing that in endemic areas percentage of serapositive birds vary from 40% to 100% with average of 77%. They further describe different levels of WNV prevalence according to immunity of hooded crows; non-endemic with 1% immunity, transition area with 31% immunity and endemic with 80% immunity. In non-endemic areas where the virus has more recently been spreading and there has not been enough time for genetic adaptation in the birds, it was found that neutralizing antibodies were detected in 23% of the resident birds in Staten Island [7] and specific anti-WNV antibodies were detected in 21% of the resident birds in the Dominican Republic [60]. In addition, WNV neutralizing antibodies in human populations showed that in non-endemic area there is 24% immunity and in endemic area 84% immunity [5]. There is not sufficient data for an accurate estimate of the number of mosquitoes per bird (m), however, we assume as a first approximation that the number increases as a function of temperature as presented in Table 1. In any case, we estimate that m and the other parameters (a, p and n) will vary similarly in both regions. The average recovery rate (r) in birds was estimated to be 0.25 since the average incubation period of WNV in a bird is thought to be about 4 days [7]. The range of temperatures was chosen to represent the entomological characteristics of transmission and mosquito’s survival.

Results and Discussion

In Figure 2 a graph of R0 as a function of temperature for both endemic and new-emergence regions is presented. Sensitivity analysis for 10% variation in temperature did not change the main result that at elevated temperatures, the new-emergence region is more susceptible to outbreaks. While in endemic regions, the values of R0 stay closer to one. When R0<1, the WNV epidemic cannot be sustained as can be seen in endemic regions at a temperature that will promote on the other hand, the propagation of the virus in new-emergence regions. According to this analysis, the higher susceptibilityof birds in new emergence areas may effect, in a complex manner, the more accelerated WNV propagation in these regions. Assuming that North America is considered to be a new-emergence area, according to the WNV R0 model, taking into account its qualitative nature, WNV will propagate there within bird populations, starting already at 25°C. In endemic regions, for example, WNV will start propagating at a temperature close to 30°C and at a lower rate. The model is irrelevant for temperature higher than 35°C due to mosquito mortality. Estimates of R0, as an indicator for WNV emergence, will be more accurate as we obtain more adequate parameter values to make better comparisons and identify locations at risk. On an annual level in the USA, there is a seasonal trend of human infection occurring from May to September – during the summer when the temperatures are obviously higher consistent with a higher R0 for the amplification cycle at elevated temperatures. This is also consistent with the findings in New England in particular in Connecticut where field-collected mosquitoes showed a high virus activity extending from early August through the end of October [61]. Once WNV emerged, it is expected that it will continue to spread in the new world over the next years, introduced primarily via migratory birds and amplified by local domestic cycles. It is likely that this virus will propagate into Central and South America, as it has already started to happen [13].


Figure 2: Indian Ayurvedic Punica is a new wonder source to combat drug resistant malaria. Also offers a paradigm shift.


Figure 3: Chemical formula is C48H28O30 and Molecular range is 1100~1125.


Figure 4: Chemical formula is C34H22O22 and Molecular range is 780~785.

New in the new world, WNV has continued to expand in the Western Hemisphere, and virus activity has been detected in Canada, Mexico and the West Indies as well. “Health Canada” reported its first WNV isolation from birds in Ontario in 2001. Four hundred cases were identified in humans in Ontario and Quebec in 2002, and by the end of 2003, disease activity had spread to a total of nine provinces and territories [62].

A similar pattern of spread has been seen in the Caribbean and Central America: WNV-neutralizing antibodies were detected in samples from birds in the Caribbean Islands in 2002 and from horses in Mexico [60,63-65]. It is likely that once introduced to a new emergence area in the Western Hemisphere, WNV will become endemic as it already happened in the Middle East. Meanwhile, new-emergence regions are more vulnerable to spread of infection, as R0 reaches a threshold of 1 at lower temperatures (Figure 2). It is clear that the expected increasing global warming will affect these regions a lot faster than the endemic ones. Although the biological components of the transmission cycle of a vector-borne disease are similar in different parts of the world, the patterns of spread differ from location to location depending on environmental conditions. Thus, as the world undergoes environmental change accompanied by global warming [66-68], the many factors contributing to the spread of vector-borne diseases, such as agricultural practices and land use will change as well [69,70]. The destruction of the natural surroundings (e.g., deforestation and desertification that accompany agricultural land development) might create new ecological conditions that will affect the distribution of birds and their penetration into new-emergence regions that, as we saw, are more susceptible to outbreaks. Here we use R0 qualitatively to compare the spread of WNV in endemic vs. new emerging regions.

The R0 equation Figure 1 does not take into account other modes of transmission that might add to the amplification such as cloacal shedding of virus (found in 17 of 24 species), oral shedding in 12 of 14 species, contact and oral transmission [7] feather-picking of sick birds [71] and non-viremic transmission via vector co-feeding [72-74]. We assume that these modes of direct transmission are marginal; however, it might have implications if we want to control the disease through vector destruction. In this paper, we use R0 solely as an effective way to explain the rapid expansion of WNV in new emergence areas. The effect of temperature on some aspects of WNV is well characterized in the literature, mostly examining one parameter at a time in a laboratory setting. In the field the entomological parameters act together along with those of host competence, as described by the equation of the basic reproductive number (R0) (Figure 1). Our estimates for infectivity of birds is based on published data as already described; moreover a 10% sensitivity analysis shows that the result is robust, that even a 10% deviation in our estimates will not change the main prediction that new-emergence regions are more vulnerable to WNV spread as a consequence of climate warming (Figure 2). Indeed, the simulations of the Basic Reproduction Number (R0) as a function of temperature sensitive parameters, showing that geographic locations within newemergence areas are more vulnerable to the spread of West Nile Virus, are consistent with the pattern of spread in the Caribbean and Central America. On the other hand the lower R0s in endemic areas are representative of the pattern of spread in Egypt and Israel. This approach might be valuable for future qualitatively comparisons of sites with different environmental parameters and predict regions at risk.


This research was funded by a grant from the Israeli Center for the Study of Emerging Diseases. In addition, we would like to thank the Kuvin Centre for the Study of Infectious and Tropical Disease in the Hebrew University, Jerusalem, for their generous hospitality. We thank Rachel Nasca and Isabel Madzorera for their editorial assistance.


  1. Smithburn JS, Hughes TP, Burke AW, Paul JH (1940) A neurotropic virus isolated from the blood of a native of Uganda. Am J Trop Med Hyg 20: 471-492.
  2. Hayes CG(1989) Thearboviruses: epidemiology and ecology.
  3. Hayes EB, Gubler DJ (2006) West Nile virus: epidemiology and clinical features of an emerging epidemic in the United States. Annu Rev Med 57: 181-194.
  4. WORK TH, HURLBUT HS, TAYLOR RM (1955) Indigenous wild birds of the Nile Delta as potential West Nile virus circulating reservoirs. Am J Trop Med Hyg 4: 872-888.
  5. HURLBUT HS, RIZK F, TAYLOR RM, WORK TH (1956) A study of the ecology of West Nile virus in Egypt. Am J Trop Med Hyg 5: 579-620.
  6. Rappole JH, Derrickson SR, Hubálek Z (2000) Migratory birds and spread of West Nile virus in the Western Hemisphere. Emerg Infect Dis 6: 319-328.
  7. Komar N, Langevin S, Hinten S, Nemeth N, Edwards E, et al. (2003) Experimental infection of North American birds with the New York 1999 strain of West Nile virus. Emerg Infect Dis 9: 311-322.
  8. Steele KE, Linn MJ, Schoepp RJ, Madon M Cossen, Woods L (2000) Pathology of fatal West Nile virus infections in native and exotic birds during the 1999 outbreak in New York City, New York. Vet Pathol 37: 208-214.
  9. Molaei G, Andreadis TG, Armstrong PM, Anderson JF, Vossbrinck CR (2006) Host feeding patterns of Culex mosquitoes and West Nile virus transmission, northeastern United States. Emerg Infect Dis 12: 468-474.
  10. Campbell GL, Marfin AA, Lanciotti RS, Gubler DJ (2002) West Nile virus.  Lancet Infect Dis 2: 519-529.
  11. SOUTHAM CM, MOORE AE (1954) Induced virus infections in man by the Egypt isolates of West Nile virus. Am J Trop Med Hyg 3: 19-50.
  12. Bunning ML Bowen RA, Cropp B, Sullivan K, Davis B, et al. (2001) Experimental infection of horses with West Nile virus and their potential to infect mosquitoes and serve as amplifying hosts. Ann N Y AcadSci 951: 338-339.
  13. Chancey C, Grinev A, Volkova E, Rios M1 (2015) The global ecology and epidemiology of West Nile virus. Biomed Res Int 2015: 376230.
  14. Lanciotti RS, Roehrig JT, Deubel V, Smith J, Parker M, et al. (1999) Origin of the West Nile virus responsible for an outbreak of encephalitis in the northeastern United States. Science 286: 2333-2337.
  15. Lvov DK, Butenko AM, Gromashevsky VL, Larichev VP, Gaidamovich SY, et al. (2000) Isolation of two strains of West Nile virus during an outbreak in southern Russia, 1999. Emerg Infect Dis 6: 373-376.
  16. Hubálek Z, Halouzka J (1999) West Nile fever--a reemerging mosquito-borne viral disease in Europe.  Emerg Infect Dis 5: 643-650.
  17. Hubálek Z (2000) European experience with the West Nile virus ecology and epidemiology: could it be relevant for the New World? Viral Immunol 13: 415-426.
  18. Nash D, Mostashari F, Fine A, Miller J, O'Leary D, et al. (2001) The outbreak of West Nile virus infection in the New York City area in 1999. N Engl J Med 344: 1807-1814.
  19. Anderson JF, Andreadis TG, Vossbrinck CR, Tirrell S, Wakem EM, et al. (1999) Isolation of West Nile virus from mosquitoes, crows, and a Cooper's hawk in Connecticut. Science 286: 2331-2333.
  20. Reisen W, Lothrop H, Chiles R, Madon M, Cossen C, et al. (2004) West Nile virus in California. Emerg Infect Dis 10: 1369-1378.
  21. Biggerstaff BJ, Petersen LR (2003) Estimated risk of transmission of the West Nile virus through blood transfusion in the US, 2002. Transfusion 43: 1007-1017.
  22. Rappole JH, Hubálek Z (2003) Migratory birds and West Nile virus. J ApplMicrobiol 94 Suppl: 47S-58S.
  23. GOLDBLUM N, STERK VV, PADERSKI B (1954) West Nile fever; the clinical features of the disease and the isolation of West Nile virus from the blood of nine human cases. Am J Hyg 59: 89-103.
  24. Cohen D, Zaide Y, Karasenty E, Schwarz M, LeDuc JW, et al. (1999) Prevalence of antibodies to West Nile fever, sandfly fever Sicilian, and sandfly fever Naples viruses in healthy adults in Israel. Public Health Rev 27: 217-230.
  25. Katz G, Rannon L, Nili E, Danon YL (1989) West Nile fever--occurrence in a new endemic site in the Negev. Isr J Med Sci 25: 39-41.
  26. Chowers MY, Lang R, Nassar F, Ben-David D, Giladi M, et al. (2001) Clinical characteristics of the West Nile fever outbreak, Israel, 2000. Emerg Infect Dis 7: 675-678.
  27. Hindiyeh M, Shulman LM, Mendelson E, Weiss L, Grossman Z, et al. (2001) Isolation and characterization of West Nile virus from the blood of viremic patients during the 2000 outbreak in Israel. Emerg Infect Dis 7: 748-750.
  28. Weinberger M, Pitlik SD, Gandacu D, Lang R, Nassar F, et al. (2001) West Nile fever outbreak, Israel, 2000: epidemiologic aspects. Emerg Infect Dis 7: 686-691.
  29. Nir Y, Goldwasser R, Lasowski Y, Avivi A (1967) Isolation of arboviruses from wild birds in Israel. Am J Epidemiol 86: 372-378.
  30. Nir Y, Lasowski Y, Avivi A, Cgoldwasser R (1969) Survey for antibodies to arboviruses in the serum of various animals in Israel during 1965-1966. Am J Trop Med Hyg 18: 416-422.
  31. Nir Y, Avivi A, Lasovski Y, Margalit J, Goldwasser R (1972) Arbovirus activity in Israel. Isr J Med Sci 8: 1695-1701.
  32. Samina I, Margalit J, Peleg J (1986) Isolation of viruses from mosquitoes of the Negev, Israel. Trans R Soc Trop Med Hyg 80: 471-472.
  33. Malkinson M, Weisman Y, Pokamonski S, King R, Deubel V (2001) Intercontinental transmission of West Nile virus by migrating white storks. Emerg Infect Dis 7: 540.
  34. Malkinson M, Banet C (2002) The role of birds in the ecology of West Nile virus in Europe and Africa. Curr Top MicrobiolImmunol 267: 309-322.
  35. Leshem Y, Yom-Tov Y (1998) Routes of migrating soaring birds. IBIS 140: 41-52.
  36. Miller BR, Nasci RS, Godsey MS, Savage HM, Lutwama JJ, et al. (2000) First field evidence for natural vertical transmission of West Nile virus in Culexunivittatus complex mosquitoes from Rift Valley Province, Kenya. Am J Trop Med Hyg 62: 240-246.
  37. Gould LH, Fikrig E (2004) West Nile virus: a growing concern? J Clin Invest 113: 1102-1107.
  38. Ebel GD, Carricaburu J, Young D, Bernard KA, Kramer LD (2004) Genetic and phenotypic variation of West Nile virus in New York, 2000-2003. Am J Trop Med Hyg 71: 493-500.
  39. Epstein PR (2001) West Nile virus and the climate. J Urban Health 78: 367-371.
  40. Lopez-Velez R, Moreno R (2005) Climate change in Spain and risk of infectious and parasitic diseases transmitted by arthropods and rodents. Rev EspSaludPublica 79: 177-190.
  41. Izmerov NF, Revich BA, Korenberg EI (2005) Climate changes and health of population in Russia in XXI century. Med Tr Prom Ekol: 1-6.
  42. Styer LM, Bernard KA, Kramer LD (2006) Enhanced early West Nile virus infection in young chickens infected by mosquito bite: effect of viral dose. Am J Trop Med Hyg 75: 337-345.
  43. Ross R(1911)The prevention of malaria. John Murray, London.
  44. Rogers DJ (1988) The dynamics of vector-transmitted diseases in human communities. Philos Trans R SocLond B BiolSci 321: 513-539.
  46. Dietz K (1993) The estimation of the basic reproduction number for infectious diseases. Stat Methods Med Res 2: 23-41.
  47. Dobson A, Foufopoulos J (2001) Emerging infectious pathogens of wildlife. Philos Trans R SocLond B BiolSci 356: 1001-1012.
  48. Bowman C, Gumel AB, van den Driessche P, Wu J, Zhu H (2005) A mathematical model for assessing control strategies against West Nile virus. Bull Math Biol 67: 1107-1133.
  49. Cornel AJ, Jupp PG, Blackburn NK (1993) Environmental temperature on the vector competence of Culexunivittatus (Diptera: Culicidae) for West Nile virus. J Med Entomol 30: 449-456.
  50. Dohm DJ, Turell MJ (2001) Effect of incubation at overwintering temperatures on the replication of West Nile Virus in New York Culexpipiens (Diptera: Culicidae). J Med Entomol 38: 462-464.
  51. Dohm DJ, O'Guinn ML, Turell MJ (2002) Effect of environmental temperature on the ability of Culexpipiens (Diptera: Culicidae) to transmit West Nile virus. J Med Entomol 39: 221-225.
  52. Martens P (1998) Health and climate change.Earhscan Publications Ltd, UK.
  53. Olejnícek J, Gelbic I (2000) Differences in response to temperature and density between two strains of the mosquito, Culexpipiensmolestusforskal. J Vector Ecol 25: 136-145.
  54. Reisen WK, Fang Y, Martinez VM (2006) Effects of temperature on the transmission of west nile virus by Culextarsalis (Diptera: Culicidae). J Med Entomol 43: 309-317.
  55. Turell MJ, O'Guinn ML, Dohm DJ, Jones JW (2001) Vector competence of North American mosquitoes (Diptera: Culicidae) for West Nile virus. J Med Entomol 38: 130-134.
  56. Turell MJ, O'Guinn ML, Dohm DJ, Webb JP Jr, Sardelis MR (2002) Vector competence of Culextarsalis from Orange County, California, for West Nile virus. Vector Borne Zoonotic Dis 2: 193-196.
  57. Jupp PG (1974) Laboratory studies on the transmission of West Nile virus by Culex (Culex) univittatus Theobald; factors influencing the transmission rate. J Med Entomol 11: 455-458.
  58. Buckley A, Dawson A, Moss SR, Hinsley SA, Bellamy PE, et al. (2003) Serological evidence of West Nile virus, Usutu virus and Sindbis virus infection of birds in the UK. J Gen Virol 84: 2807-2817.
  59. Lord CC, Day JF (2001) Simulation studies of St. Louis encephalitis and West Nile viruses: the impact of bird mortality. Vector Borne Zoonotic Dis 1: 317-329.
  60. Komar O, Robbins MB, Klenk K, Blitvich BJ, Marlenee NL, et al. (2003) West Nile virus transmission in resident birds, Dominican Republic. Emerg Infect Dis 9: 1299-1302.
  61. Andreadis TG, Anderson JF, Vossbrinck CR, Main AJ (2004) Epidemiology of West Nile virus in Connecticut: a five-year analysis of mosquito data 1999-2003. Vector Borne Zoonotic Dis 4: 360-378.
  63. Dupuis AP, Marra PP, Kramer LD (2003) Serologic evidence of West Nile virus transmission, Jamaica, West Indies. Emerg Infect Dis 9: 860-863.
  64. Quirin R, Salas M, Zientara S, Zeller H, Labie J, et al. (2004) West Nile virus, Guadeloupe.Emerg Infect Dis 10: 706-708.
  65. Loroño-Pino MA, Blitvich BJ, Farfán-Ale JA, Puerto FI, Blanco JM, et al. (2003) Serologic evidence of West Nile virus infection in horses, Yucatan State, Mexico. Emerg Infect Dis 9: 857-859.
  66. Harrigan RJ, Thomassen HA, Buermann W, Smith TB (2014) A continental risk assessment of West Nile virus under climate change. Glob Chang Biol 20: 2417-2425.
  67. Crowder DW, Dykstra EA, Brauner JM, Duffy A, Reed C, et al. (2013) West nile virus prevalence across landscapes is mediated by local effects of agriculture on vector and host communities. PLoS One 8: e55006.
  68. Lambin EF, Tran A, Vanwambeke SO, Linard C, Soti V (2010) Pathogenic landscapes: Interactions between land, people, disease vectors, and their animal hosts. International Journal of Health Geographics 9: 54.
  69. Awerbuch T, Kiszewski AE, Levins R (2002) Surprise, non-linearity and complex behavior. In:Martins, McMichael, editors. Environmental Change, Climate and Health. Cambridge, UK.
  70. Watson TR, Patz J, Gubler JD, Parson AE, Vincent HJ (2005) Environmental health implications of global climate change. J Environ Monit 7: 834-843.
  71. Banet-Noach C, Simanov L, Malkinson M (2003) Direct (non-vector) transmission of West Nile virus in geese. Avian Pathol 32: 489-494.
  72. Higgs S, Schneider BS, Vanlandingham DL, Klingler KA, Gould EA (2005) Nonviremic transmission of West Nile virus. ProcNatlAcadSci USA 102: 8871-8874.
  73. Paz S (2006) The West Nile Virus outbreak in Israel (2000) from a new perspective: the regional impact of climate change. Int J Environ Health Res 16: 1-13.
  74. Peterson AT, Vieglais DA, Andreasen JK (2003) Migratory birds modeled as critical transport agents for West Nile Virus in North America. Vector Borne Zoonotic Dis 3: 27-37.
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  1. Audrey Smith
    Posted on Jul 19 2016 at 5:17 pm
    Malaria is a life-threatening blood disease caused by parasites transmitted to humans through the bite of the Anopheles mosquito. Once an infected mosquito bites a human and transmits the parasites, those parasites multiply in the host's liver before infecting and destroying red blood cells. The disease can be controlled and treated if diagnosed early on. Unfortunately, this is not possible in some areas of the world lacking in medical facilities, where malaria outbreaks can occur. This surely is a informative study and new approach towards malaria prevention but I hope they do even more research so it does not have any adverse effects on the ecology. Mosquito larvae must be feeding quite a number of other birds, amphibians, etc.

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