Have the 10 Plagues Happen Again?
Yale J Biol Med. 2008 Mar; 81(1): 31–42.
Published online 2008 Jul.
Origin of the Old Testament Plagues: Explications and Implications
Due north. Joel Ehrenkranz
aEmeritus Director, Florida Consortium for Infection Command
Deborah A. Sampson
bBanana Professor, University of Michigan School of Nursing
Abstract
Analyses of by disasters may supply insights to mitigate the touch on of recurrences. In this context, we offer a unifying causative theory of Onetime Testament plagues, which has nowadays day public health implications. We propose the root cause to accept been an aberrant El Niño-Southern Oscillation teleconnection that brought unseasonable and progressive climate warming forth the ancient Mediterranean coastal, including the coast of biblical Egypt, which, in plough, initiated the serial catastrophes of biblical sequence — in particular arthropod-borne and arthropod-caused diseases. Located beyond the boundary of focal climatic change, inland Goshen would non have been similarly affected. Implicit in this analysis is a framework to consider a possibility of nowadays twenty-four hours recurrence of similar catastrophes and their impact upon essential public services.
Introduction
The vivid Erstwhile Testament saga of the 10 plagues that devastated the land of Egypt and its people (Exodus ane-12) has intrigued some to seek rational explanations for a chronicle of disasters that befell 1 population however spared another. Indeed, biblical scholars in a 21st century translation of the Onetime Testament concede that from an historical standpoint, the first 9 plagues resemble natural events well known in the Middle East, salve for their patterns and rapid succession [1]. In light of present mean solar day knowledge, we offer a fresh, cohesive, and rational explanation of these events, with the implication that they could recur. The 10 plagues are: 1. the Nile River turns bloody, fouling drinking water and killing fish. 2. Frogs leave the Nile for dry country, invade Egyptian homes and dice, causing a great stench. three. Annoying small insects swarm. 4. Abrasive large insects swarm. 5. An epizootic kills different types of livestock in pasture. 6. Boils afflict beasts and humans. seven. An especially astringent thunderstorm with lightning and hailstones destroys crops about harvest. viii. Stiff winds behave swarms of locusts to obliterate remaining crops. 9. "Palpable darkness" obscures all light. ten. Firstborn Egyptians and their surviving firstborn animals die, while Israelites and their livestock live.
Brief Literature Review
In parallel with scientific advances, succeeding authors accept offered progressively rational explanations for the plagues, as well summarized by Marr and Malloy [2]. Over the past half-century, authors of four key papers accept put forwards competing scientific views. These are characterized past differing suggestions for origins of plagues 1 and v, and whether at that place was a common source for some plagues, or alternatively series connections between them. In the late 1950s, Hort attributed the bloody appearance of the Nile River and the fish kill of plague i to ruby-red silt and freshwater flagellates (Euglenia sanguinea, Haematococcus pluvialis) beingness carried downstream by torrential waters to overflow onto the overflowing plain of the Nile Delta [3,four]. She proposed that the unusually strong river overflow caused anthrax spores in contaminated soil to germinate and initiate the epizootic of plague 5 and attributed all but the hail of plague 7 to Nile overflow. Several decades later, Schoental suggested that red tide due to pigment-producing marine dinoflagellates was responsible for the encarmine Nile and fish impale. She, however, proposed a sequential plague connection, eastward.g., the flies of plague iv transmitting an unknown infectious agent to crusade plague five [v]. Hoyte, in 1993, postulated different fresh water dinoflagellates (Gymnodinium and Glenodinium sp.) equally causing plague 1, but agreed with Schoental that the flies of plague four transmitted the agent of plague 5, and also caused plague six [6] Every bit origin of plague 5, Hoyte rejected previously suggested bacterial and viral agents — including Bacillus anthracis and Rift Valley fever virus (RVFV) — based upon differing livestock susceptibilities to infectious agents, offering instead the protozoon, Trypanosoma evansi. Thereafter, Marr and Malloy suggested a different species of freshwater dinoflagellates (cyanobacteria) for plague ane and made a connexion with plague 2 by proposing that dinoflagellate toxins forced frogs to flee the river. Moreover, they presented a model in which each of the first 9 plagues shaped the next, thereby greatly advancing the concept of sequential plague causation. They also revived consideration of viral origin for plague 5 by suggesting that ii viruses — African horse sickness and Bluetongue — were responsible, having been spread by vector insects of plague 3 [2]. In contrast to varying opinions as to plagues 1 and five, authors of the three papers addressing plague 9 all agreed the cause was a sandstorm [two,4,6]. Therefore, while differing in detail, previous scholars have considered that living agents and abnormal climatic conditions (as well manifested in the hail of plague 7 and the winds of plague 8) account for the first nine plagues.
It is the 10th plague — the seemingly inexplicably pattern of selective killing of Egyptian firstborn humans and animals yet sparing all Hebrew humans and animals — that has posed the thorniest trouble for rational elucidation. Attempts to explain plague ten vary greatly. Hort essentially avoided the issue past proposing translation and transcription errors. In her view, the original Quondam Attestation concept of this plague was the "destruction of the first-fruits" — significant crops, not children. Hoyte also downplayed the significance of firstborn deaths, maintaining it was symbolic for the expiry of the pharaoh's eldest son from typhoid fever. (Hoyte also took note of hyperbole or poetic license in quantitative biblical descriptions, eastward.yard., death of "all" animals or contamination of "all" waters, equally practice current biblical scholars [vii]). Somewhat more creatively, Schoental, and later Marr and Malloy, argued that the firstborn died from lethal mycotoxins (e.k., Stachybotrys atra) arising in moldy granaries. The latter argued that primogeniture permitted firstborn humans to have had starting time and greatest exposure to the moldy nutrient, as did dominance for firstborn animals. They attributed survival of younger man and creature siblings to their prompt perception and avoidance of dangers lurking in moldy granaries — merely offered no support.
There is also contention every bit to the location of the biblical land of Egypt: Hort considered it to take been the whole Nile valley every bit far s as ancient Nubia, whereas Hoyte argued that the Hebrews of the Old Testament would have perceived information technology just as the Nile Delta. In either consequence, it would have likely included the places of forced Hebrew labor at the "treasure cities" of Rameses and Pithom in the northeastern Nile Delta and Egyptian dwelling places shut to the Mediterranean coast (Figure) [seven-nine]. Past dissimilarity, scholars generally concord that the part of the land of Egypt known as the region of Goshen would have been further inland, north of present twenty-four hour period Wadi Tumilat and under desert climate influences [2,3,7]. Situated at a periphery of the coastal plain, Goshen would have been a pastureland for settled and transient foreigners, including semi-nomadic Hebrew herders.
A composite representation of the aboriginal eastern Nile Delta (not to scale) that indicates the proposed full general locations of biblical sites and a diagram (to scale) of the nowadays solar day region [derived from information in eight,9,10]. As a port city, Rameses would have had direct access to one of the ancient branches of the Nile River shown north of modernistic Cairo.
Addressing the central biological or weather upshot in each plague, we now offer a fresh caption of both remote and proximate causation, based on historical examples of comparable catastrophes. We also put forward a simple biological explanation for the seemingly inexplicable 10th plague.
Focal Climate Change Proposal of Causation
Drawing from present mean solar day noesis of the interplay of climatic conditions, ecological changes, and arthropod-borne and arthropod-acquired diseases, nosotros suggest that the firsthand crusade of all plagues — in biblical sequence — was unseasonable and progressive climate warming along the eastern Mediterranean coast where Israelites worked in forced labor. The seminal event for the warming would have been an El Niño-Southern Oscillation (ENSO) teleconnection. The inland region of Goshen — beyond the climate warming — substantially would take escaped the unseasonable furnishings.
The El Niño warming component of the ENSO cycle occurs when the Southern Oscillation reverses the usual low atmospheric pressure arrangement over the western Pacific Ocean to the east, thereby raising surface temperatures of the primal and eastern Pacific in the tropics and atmospheric temperatures of adjacent country masses. This climatic event may go beyond the torrid zone, as when an El Niño warms the eastern Mediterranean bowl during late wintertime and early spring [10]. Hence, biblical Egypt as perceived by Hebrews at labor in "treasure cities" near the Mediterranean coast (Figure) would accept been in a credible location to experience ENSO-induced climatic warming. In Africa, India, South America, and Red china, ENSO atmospheric warming has caused heavy rainfall; mosquito-borne outbreaks of Rift Valley fever (RVF), malaria, and dengue; explosion of swarming locusts; and an historically severe red tide causing massive fish kills [11-16]. Indeed, a disaster of biblical proportions began in littoral Peru in March 1925 when an ENSO warmed the surface of the eastern Pacific Ocean and raised the ambient temperature of adjacent coastlands from 15° to 26° C over some three months, bringing deluging pelting to a usually barren region [12,xiv]. Large numbers of frogs, dragonflies, crickets, and mosquitoes appeared and were followed past epidemic diseases — seemingly dengue and malaria. It is noteworthy that climate warming alone, without pelting, may initiate outbreaks of musquito-borne illness. This repeatedly occurred in Colombia during the last decades of the 20th century when ENSO-induced increases in ambient temperature together with drought led to stagnation of moving rivers, breeding of vector mosquitoes, and outbreaks of dengue and malaria [17].
Administrative Bibles and Translation Inconsistencies
For consistency, we used the well-recognized and administrative sources of two dissimilar translations of the Old Attestation published in the 20th and 21st centuries by the Jewish Publication Guild [eighteen,xix]. Since not all scholars agree that the discussion choices in these translations reverberate the original Hebrew text, we also include independent scholarly opinion (personal communication, Ms. Janice Friend). The cause of plague 3, 'kinim' (phonetically) has been interpreted to hateful either gnats or lice, and is translated as "gnats" in the 20th century edition and "vermin" in the 21st, the latter adding in notation that 'kinim' is a non-specific description of small insects including mosquitoes and lice. Notwithstanding, in the Hebrew text 'kinim' is used in two ways (Exodus 8:12-xv): 'ha'aretz five'haya 50'kinim', [take the staff and strike the earth and in that location will be 'kinim'] and 'v'lo yacholu vat'hi hakinim ba'adam uvab'haima' [and the 'kinim' ate or chip both man and beast].
There is even less unanimity for the translation of 'arov,' the cause of plague four (Exodus eight:17-20): 'tishachet ha'aretz mip'nai he'arov' [the state was devastated {destroyed, decayed, or spoiled} in the face of the 'arov']. The 20th century version translates 'arov' as "swarms of flies;" the 21st as "swarms of insects," calculation in note that the meaning is uncertain. Some rabbinic scholars consider the meaning to be flies; others, wild fauna based in part on a literal interpretation of Psalm 78:45. "He sent among them swarms of 'arov', which devoured {scrap or ate} them; and frogs, which destroyed them." Most Hagaddot, however, interpret 'arov' to hateful flies as practice seven of 9 articles addressing plague iv in literature reviewed past Marr and Malloy [2].
We take 'kinim' to mean various small, annoying insects including mosquitoes and midges, and 'arov' as a contrasting general term for larger organisms, especially flies.
At that place are too differences in translations in plagues 5 and 10 equally to the subjects of epizootic disease. The 20th century translation employs "cattle" in both; even so, the 21st century version uses "livestock" in plague five and "cattle" in plague 10. In the Hebrew text, plague 5 is visited upon beasts or a group of animals as 'b'mikn'cha asher basadei, basousim, bachamorim, bag'malim babakar ovatzon' [among your herds, amidst your horses, donkeys, camels, cattle and sheep] (Exodus 9:3). The victims in plague 10 are 'b'heima' as in 'kol b'chor b'heima' [every firstborn among the beasts] (Exodus 12:29) and 'mayadam 5'advertisement b'heima h' [among men and among beasts] (Exodus 12:12). The word 'b'heima' is used throughout Exodus eleven and 12 as meaning beasts.
We take "cattle" to be a generic term for two singled-out collections of livestock: animals in pasture that are killed in plague 5 and animals destroyed in plague 10 that are located elsewhere — presumably at Egyptian dwellings.
ENSO Effects and the First Six Plagues
Every bit a parallel to the 1925 Peruvian and more contempo ENSO episodes, unseasonable and progressive focal climate warming would have lasted two to three months. This bridge would have permitted a biblical perspective of plagues as a chain of successive, and somewhat overlapping, disasters. Coinciding with the start of the lambing season and the later celebration of Passover, plague 1 would have begun nigh the vernal equinox equally the ENSO teleconnection raised ambient temperatures to a higher place 20° C. Plague 6 would have occurred i to ii months afterwards, when continued warming brought daily temperature highs higher up 23° C. At that fourth dimension, tropical ocean temperatures ordinarily would have been less than 18° C during March and libation than now, according to a paleoclimatological model [20].
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1. Water temperatures rising higher up 18° C at ancient debouching branches of the Nile River would accept stimulated growth of dinoflagellates cysts equally has historically occurred in the harbor of Alexandria, Egypt [21,22]. Alexandrium miniutum grows well in waters of depression salinity having input of nutrient-rich freshwater, conditions probable to have obtained in biblical times at the outflow of the Nile at its tardily winter-early spring depression as human and fauna waste material and other sewage flowed toward the confined estuary. When temperatures exceeded xx° C, eutrophication and nutrient upwelling would accept promoted massive algal blooms of red tide and their toxins. Prevailing onshore due north winds would have blown the toxic blooms upriver, causing its bloody advent, fouled drinking water, and fish kill.
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two. Increasing h2o temperatures would accept stimulated activity of frogs (e.g., Rana ridibunda [23]), and the toxic river environment would take forced agile frogs to flee to land. Toward nightfall every bit temperatures fell, the frogs would have sought warmth in human dwellings; subsequently, lethargic and dehydrated, they would have succumbed to opportunistic infection [v]. Anaerobic bacteria growing in frog carrion would have made the land stink.
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3. Continued atmospheric warming would accept fostered breeding in swampy areas of various abrasive pocket-size insects such every bit bitter midges (Culicoides species) and sand flies (Phlebotomus species). Culex, Aedes, and other mosquitoes would accept hatched in irrigation ditches virtually pastures — some to become virus vectors in plague 5 [24-26].
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four. Biting flies, having hatched in soil heavily polluted with fauna urine and feces, also would take become arable with warming weather. As noted past others, stable and black flies (including Stomxys and Simulian species) would have been peculiarly bothersome [two,3,vi]. Eggs of some non-biting flies would have hatched on or about animals or humans — in bedding or apparel; their larvae, being capable of growth in mammalian tissue, would afterwards cause plague 6 [27].
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5. Concurrent RVFV infection in ruminants and Westward Nile virus (WNV) in equine species would account for the epizootic of plague 5, having been freshly introduced into the Delta at a time when neither had been nowadays for 10 to 20 years. At temperatures generally ranging betwixt 20° C and 22° C, vector mosquitoes systematically and slowly would have spread both viruses to livestock throughout the pastures, eventually infecting the vast majority. Mature Egyptian herdsmen exposed in the pastures would have been unaffected, having acquired active immunity in long-past exposures [28,29]. In historic times, both RVFV and WNV intermittently have been introduced into the Nile Delta without becoming established for long periods: RVFV episodically has been transported with infected livestock, and WNV intermittently spread by infected birds [30,31].
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6. After hatching, specific fly larvae would burrow into pare and subcutaneous tissues of livestock and humans and develop in situ to cause furuncular myiasis, manifested every bit inflammatory nodules or boils. Historically in Arab republic of egypt and Saudi arabia, several species have caused myiasis in camels, goats, and sheep [27]. In humans, the tumbu fly (Cordylobia anthropophaga) has played a office [32,33]. Tumbu fly larvae often produce myiasis in legs and buttocks, which might explain the biblical observation that Egyptian "magicians could not stand before Moses because of the boils" [34].
ENSO Effect and the Last Four Plagues
By late April or May, progressive rises in littoral warming would accept brought daily high temperatures above 25° C to initiate a supercell storm and cause plague 7. Every bit rise temperatures progressed and daily highs forth the coast approached 29° C, lasting effects of plague vii would set atmospheric condition for plagues 8 to 10.
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seven. Severe springtime storms occasionally arise in the Eye East. A dangerous hailstorm occurred in Arab republic of egypt as recently as 1999 [35,36]. The tempest of plague 7 was particularly severe, bringing hailstones "such as had not fallen upon Arab republic of egypt since it had become a nation." It would have started every bit warm, moist sea air moving over the northern Delta collided with cool, dry inland air, causing thunder, lightning, heavy rains, and then large hailstones, destroying crops nearly harvest. Later, the storm would have left puddles of rainwater and promoted new vegetation from pastures to dwelling places.
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viii. Violent tempest winds blowing start east and and then due west from the desert would take, respectively, conveyed swarms of desert locusts (Schistocerca gregaria) into and out of coastal Arab republic of egypt. An exact parallel occurred in 1967, as swarming desert locusts were showtime brought to the seacoast of Egypt from the Arabian Desert by a cyclonic east air current, and then carried away by a similar west wind [37].
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nine. Every bit violent storm winds subsided, prevailing warm bounding main winds laden with wet would take returned to the northern Delta to overlay cool desert air left by plague eight. Condensation of wet would yield a dense advection fog. This sea fog would have obscured all calorie-free along the coast. Absent-minded dissipating wind or air shift for three days, darkness would have persisted. Dense fogs in Egypt have caused multiple fatal vehicular accidents as recently as 2006 [38].
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10. New vegetation and h2o puddles resulting from the storm of plague seven would take promoted breeding of mosquitoes and attracted birds. With ambient temperatures approaching 29° C, both Aedes and Culex mosquitoes would have become increasingly efficient for disseminating RVFV, and Culex species for disseminating WNV to Egyptian inhabitants of humble and palatial dwellings [39,xl]. Immune mature Egyptians would take survived exposures to both viruses [xxx,31]. Non-immune younger Egyptians (including firstborn) and domiciled livestock would have died from ane or the other.
Discussion
Disturbed climatic conditions over the biblical land of Egypt conspicuously are evident in the Old Attestation account of plagues seven and eight, bespeaking the turbulent atmospheric events of a supercell storm bearing hailstones to destroy crops and veering winds to drive swarms of locusts to and fro. Unseasonable springtime warming would accept precipitated such a storm, like the thunderstorm over the Sinai desert of Egypt in Apr 1998 occurring later an unusual one-week estrus wave [35]. To account for an extended two- to three-month menstruation of unseasonable climate warming that would take led to the succession of plagues, it is necessary to infer a more extraordinary climatic miracle. We brand the case that the seminal event was an ENSO teleconnection, causing progressive warming along the Mediterranean coast of biblical Egypt for such duration. Goshen, lying beyond the purlieus of climate change, would thereby escape all or most plagues.
The description of the x plagues depicts an increasingly severe sequence of public health catastrophes: ruddy tide and its toxic sequels of fish kill, water pollution and expulsion of frogs from the Nile; explosions of diverse arthropod populations; two episodes of epizootic and epidemic diseases (the second causing deaths of firstborn); a turbulent atmosphere with thunder, lightening, rain and hail, and then trigger-happy winds; and loss of daylight. Historical records of catastrophes occurring afterwards atmospheric disturbances caused by ENSO teleconnections mirror the Onetime Attestation business relationship, salvage for hail and loss of daylight [16,eleven-xv,17]. We propose that the hail and loss of daylight also had an ENSO origin in a supercell storm. The One-time Attestation tape provides an opportunity to consider the breadth of public services that might exist required in outcome of another series of ENSO calamities. Were a populous region to at present be struck with catastrophes that parallel the biblical elements, essential public wellness, medical, and veterinary services likely would exist overwhelmed. In fact, as grooming for agin public health effects of climate change, Fromkin and colleagues at the U.South. Centers for Affliction Control and Prevention are calling upon public health policymakers and professionals at all levels to plan coordinated responses [41]. In event of sustained increases in mean ambient temperatures, they anticipate a take a chance of tropical arthropod-borne infectious diseases, including RVFV and WNV outbreaks, and propose both surveillance of vector-borne diseases and the potential-for-vector-borne-diseases, the latter to be done by monitoring temperature, rainfall and vector populations.
Virus Diseases, Livestock Stress and Plague v
Bunyavirus and flavivirus outbreaks have been documented afterwards an ENSO cycle [11,17]. Neither RVFV (a bunyavirus) nor WNV (a flavivirus) solitary tin account for affliction in all livestock types enumerated in plague v. Whereas WNV infection often may be fatal to equines [42], nosotros find no reports of WNV infection causing serious disease, let lone expiry, in developed camels. In contrast, RVFV infection is often deadly for many ruminant species, but does not cause clinical signs in equines [43]. Some young ruminants are especially susceptible to RVFV: The bloodshed rate of infection for newborn lambs is greater than xc percent, whereas for sheep it is xxx percentage [44]. Salubrious mature camels usually manifest no clinical findings of RVFV infection, save ballgame [5,43,45]. When severely stressed, however, camels may die from RVFV infection. Early on in the 1977 RVF outbreak in Egypt, at that place were 39 implicated RVFV deaths in 40 camels in transit from the Sudan; the animals as well suffered trypanosomiasis and starvation [46,47]. Ultimately, this lot accounted for 69 per centum of all 56 camel deaths in the outbreak [47]. Again in the 2000 Saudi Arabian RVF outbreak, deaths of tens of thousands of infected camels and other livestock occurred amongst livestock in transport at the Cherry Sea port of Jazan [48]. In both outbreaks, RVFV infection was the proverbial "last harbinger" for the camels — the ultimate in a concatenation of stresses that accompany livestock transportation [49]. In the Former Testament chronicle, RVFV infection would have been the ultimate stress for camels and other ruminants in pasture — already suffering exposure to inclement weather, parasitic infestations, malnutrition owing to poor quality of late wintertime pasturage, and dehydration due to the limited water in irrigation ditches at seasonally low levels. Livestock recently acquired from nomadic caravans additionally would have borne stresses inherent to transportation. Among severely stressed biblical equines, the virulence of WNV infection also would take been enhanced, as has been demonstrated in laboratory animals [50].
Epidemiology and Pathogenesis of Plague 10
The ancient and continuing Egyptian practice of stabling livestock within dwellings would accept facilitated human contact with RVFV-infected livestock [29]. Since RVFV may be secondarily spread by directly contact, susceptible biblical Egyptians would have become infected at their homes during care or butchering of RVFV-infected animals, equally well every bit through directly contact with infected persons [51,52]. They too would have been exposed to RVFV through milk of infected animals — in pastoral communities, milk is still a nutrient staple. Moreover, RVFV and some strains of WNV may cause fulminating hepatic and/or hemorrhagic disease in humans [46,52-55]. When hepatic disease was a characteristic of fatal human RVFV infection, autopsies in Egypt often showed advanced schistosomal cirrhosis [56]. Every bit schistosomiasis was owned among aboriginal Egyptians, hepatic cirrhosis due to schistosomiasis would have been expected [57]. Fulminating RVFV or WNV infection superimposed upon preexisting hepatic cirrhosis would have been rapidly lethal to susceptible biblical Egyptians [53]. Finally, to the extent it was prevalent, a specific genetic characteristic among not-immune biblical Egyptians — the defective CCR5 allele leading to absence of chemokine receptor CCR5 — would have increased fatal outcomes of WNV infection [58].
In those parts of Africa where RVFV and WNV were enzootic during the 20th century, the prevalence of antibodies to each, although widespread, was low in persons younger than xv to 20 years [xxx,31]. Lacking the active amnesty of mature elders, firstborn biblical Egyptian children exposed to RVFV through contact or to either virus through mosquito transmission would take been unprotected from lethal infection. Conversely, younger siblings still or recently at breast, possessing transplacental passive immunity, would have been protected. Such a dramatic contrast would accept fostered the perception of vulnerability of the firstborn in plague 10.
Eventuation of Plague 5 into Plague 10
Residue furnishings of the heavy rains of plague 7 would have extended the geographical range of transmission of both viruses from pastures to human habitations. Close to abode places of the biblical Egyptians, new vegetation and standing water would have increased vector mosquito numbers and attracted birds [59,60]. Effectually the dwellings, infected birds would have amplified WNV, and infected lambs would accept amplified RVFV. In plague 10, the contrast in mortalities of RVFV-infected lambs with RVFV-infected sheep near homo dwellings — absent stresses of pasture life — would accept lent a perception of widespread deaths among firstborn animals.
As atmospheric warming continued, the end result of masses of newly hatched vector mosquitoes nearly Egyptian dwellings chop-chop amplifying both viruses, in concert with secondary contact spread of RVFV, would have been the devastating plague x. At the fourth dimension of plague 5, postulated ambient temperatures greater than 20° C merely less than 23° C would have permitted Aedes and Culex mosquito vectors to steadily — just not rapidly — transmit RVFV among pastured ruminants, and Culex species to slowly spread WNV from flocks of nearby birds to grazing equines. Connected climbing temperatures, forth with many more mosquito vectors, would have accelerated transmission of both viruses; at ambient temperatures of 26° C, these mosquitoes would have become very efficient transmitters [39,40]. Historically, some menstruum of warm weather is necessary for introduced RVFV to develop into a major outbreak. RVFV was brought into Egypt in 1977 and spread northward largely unnoticed through the summertime and early autumn; in Oct, it exploded into an epidemic and epizootic in the Nile Delta [25,46,47]. Similarly, RVFV was identified in Saudi Arabia in mosquitoes in 1999, nevertheless was recognized every bit an epidemic and epizootic only in August-September 2000 [48,61]. Along this line, experimental findings demonstrate a demand for physical warming of vector mosquitoes for WNV manual. No WNV could be recovered from virus-inoculated Culex mosquitoes held at 10° C; withal, WNV was recovered from comparably inoculated mosquitoes additionally warmed to 26° C for three to six weeks [62].
Absent similar climatic conditions in Goshen, comparable disasters would non accept occurred. Interestingly, recent studies in the Nile Delta utilizing the newer technique of thermal scanning radiometry correlate the focal distribution of filariasis, a disease also transmitted by Aedes, Culex, and other mosquitoes, with focal surface and subsurface moisture in the soil and plant canopy [63]. This finding lends support to the view that the occurrence of the 10th plague in the state of Egypt, only non in Goshen, may have been due in large part to focal differences in moisture.
That overlapping mosquito-borne outbreaks of virus disease practise occur was repeatedly documented in episodes caused by Western encephalitis and St. Louis encephalitis viruses in Kern Canton, California, during the latter decades of the 20th century [64]. Recovery of WNV from mosquitoes in a setting of enzootic RVF in Mauritania in 1987 and at the end of an RFV epidemic in Egypt in 2002 provides historical support to the concept that these viruses together could have caused plagues 5 and 10 [65,26]. Additionally, observations made during an RVF outbreak in Islamic republic of mauritania in 1988 seem relevant: Equally expected, the finding of icterus was significantly greater among persons with laboratory evidence of recent RVFV infection than in those without [52]. Notwithstanding, this was non the case for individuals having hemorrhagic signs, which led the seasoned investigators to consider the possibility of an boosted outbreak agent.
Conclusions and Outlook
The present analysis of the origin of the Old Testament plagues offers a possible unifying theory of interrelation of a single atmospheric event with a serial of unseasonable climate changes causing all calamities. Continuing scientific advances may permit future development of a formal hypothesis based on our analysis. one) Directions for new inquiry could include new scientific investigations to explore possibilities of ENSO occurrences having caused major climate changes along the southeastern Mediterranean littoral during biblical times — electric current measurement of flood heights of the Nile River and tree ring widths in Asia forth with analyses of ice core samples offer climate estimates of only the past 500 years [66]. New measurements of isotope tracers in banded reef coral in the Cherry-red Sea and temperature at diverse depths in the globe's surface might reconstruct before climatic conditions and permit estimations of variations across a range of inter-seasonal to inter-decadal periods in ancient times [x]. 2) If nucleic acids from mummified humans and animals permitted reconstruction of viruses, this might shed calorie-free on origins of epidemics and epizootics in biblical Egypt [67]. 3) Continuing studies of historical descriptions in aboriginal written sources could yield new insights into gimmicky climatologically related wellness risks.
Outbreaks of arthropod-viruses are documented throughout tropical and subtropical regions post-obit ENSO atmospheric reversals [xi,thirteen,xiv,17]. Recent dissemination of so-called "tropical" viruses such as Bluetongue, Chikungunya fever, and WN has resulted in autochthonous infections in mid-breadth zones [68-70]. In future ENSO cycles, such viruses may be important public health concerns in temperate regions.
Acknowledgments
We thank Dr. Charles Calisher and Dr. John S. Marr for review of the manuscript, and Mr. David Weiss for his invaluable library guidance.
Abbreviations
| RVF | Rift Valley fever |
| RVFV | Rift Valley fever virus |
| ENSO | El Niño-Southern Oscillation |
| WNV | West Nile virus |
References
- Berlin A, Brettler MZ. The Jewish Study Bible. The Jewish Publication Society Tanakh Translation. New York: Oxford University Press; 2004. Annotation seven.14-10.9: The commencement nine plagues; p. 117. [Google Scholar]
- Marr JS, Malloy CD. An epidemiological assay of the ten plagues of Egypt. Caduceus. 1996;12:7–24. [PubMed] [Google Scholar]
- Hort K. The Plagues of Egypt. Zeitschrift fur die Alttestamentliche Wissenschaft. 1957;69:84–103. [Google Scholar]
- Hort G. The Plagues of Egypt Two. Zeitschrift fur die Alttestamentliche Wissenschaft. 1958;70:48–59. [Google Scholar]
- Schoental R. Mycotoxins and the bible. Perspect Biol Med. 1984;28:117–120. [PubMed] [Google Scholar]
- Hoyte MMD. The Plagues of Egypt: What killed the animals and the firstborn? Med J Australia. 1993;158:706–708. [PubMed] [Google Scholar]
- Berlin A, Brettler MZ. The Jewish Written report Bible. The Jewish Publication Society Tanakh Translation. New York: Oxford University Press; 2004. Notation 12.29-42: The tenth plague and the Exodus; pp. 128–129. [Google Scholar]
- CIA. The World Factbook — Egypt [Cyberspace] [updated 13 December 2007; cited 2007 Dec 25]. Bachelor from: https://www.cia.gov/library/publications/the-globe-factbook/geos/eg.html.
- Sarna NM. Exploring Exodus. New York: Shocken Books; 1996. Introduction; pp. 1–14. [Google Scholar]
- Alpert P, Baldi M, Ilani R, et al. Relations between climate variability in the Mediterranean region and the tropics: ENSO, south Asian and African monsoons, hurricanes and Saharan grit. In: Lionello P, Malanotte-Rizzoli P, Boscolo R, editors. Mediterranean Climate Variability, four. Amsterdam: Elsevier; 2006. pp. 149–177. [Google Scholar]
- Linthicum KL, Anyamba AA, Tucker CJ, et al. Climate and satellite indicators to forecast Rift Valley fever epidemics in Kenya. Scientific discipline. 1999;285:397–400. [PubMed] [Google Scholar]
- Nials FL, Deeds EE, Moseley ME, et al. El Nino: the catastrophic flooding of Republic of peru. Part II. Field Museum of Natural History Message. 1979;50:4. [Google Scholar]
- Bouma MJ, van der Kaay HJ. The El Niño Southern Oscillation and the Celebrated Malaria Epidemics on the Indian Subcontinent and Sri Lanka: An Early Warning Arrangement for Future Epidemics? Trop Med & Internat Health. 1996;1:86–96. [PubMed] [Google Scholar]
- Nash JM. El Nino: Unlocking the Secrets of the Main Atmospheric condition-maker. New York: Warner; 2002. pp. 168–179. [Google Scholar]
- Todd MC, Washington R, Cheke RA, et al. Dark-brown locust outbreaks and climate variability in southern Africa. J Applied Environmental. 2002;39:31–42. [Google Scholar]
- Yin K, Harrison PJ, Chen J, et al. Red tides during spring 1998 in Hong Kong: is El Niño responsible? Mar Ecol Prog Ser. 1999;187:289–294. [Google Scholar]
- Poveda Thou, Graham NE, Epstein PR, et al. Climate and ENSO variability associated with vector-borne diseases in Columbia. In: Diaz HF, Margraf 5, editors. El Niño and the Southern Oscillation. Multiscale Variability and Global and Regional Impacts. Cambridge, U.k.: Cambridge University Press; 2000. pp. 183–204. [Google Scholar]
- Jastrow 1000, editor. The Holy Scriptures According to the Masoretic Text. Philadelphia: The Jewish Publication Society of America; 1955. Exodus 1:1-12:35; pp. 72–88. [Google Scholar]
- Berlin A, Brettler MZ, editors. The Jewish Study Bible. The Jewish Publication Society Tanakh Translation. New York: Oxford University Press; 2004. Exodus 1:one-12:35; pp. 107–130. [Google Scholar]
- Trenberth KE, Otto-Bliesner BL. Toward integrated reconstruction of by climates. Scientific discipline. 2003;300:589–590. [PubMed] [Google Scholar]
- Global Invasive Species Database. Alexandrium minutum (algae) [database on the Internet] [cited 2007 November 7]. Available from: http://www.issg.org/database/species/environmental.asp?si=1023&fr=1&sts=sss&lang=EN.
- Ismael AA, Khadar AM. Alexandrium minutum cysts in sediment cores from the eastern harbour of Alexandria, Egypt. Oceanologia. 2003;45:721–731. [Google Scholar]
- Akef MMS, Schneider H. The eastern class of Rana ridibunda (anura: ranidae) inhabits the Nile delta. Zoologischer Anzeiger. 1989;223(3/four):S129–S138. [Google Scholar]
- Hurlburt HS, Weitz B. Some observations of the bionomics of the common mosquitoes of the Nile delta. Amer J Trop Med Hyg. 1956;vi:901–908. [PubMed] [Google Scholar]
- Meegan JM. Rift Valley fever epizootic in Egypt: 1. Clarification of epizootic and virologic studies. Trans Roy Soc Trop Med Hyg. 1979;73:618–623. [PubMed] [Google Scholar]
- Turell MJ, Morrill JC, Rossi CA, et al. Isolation of West Nile and Sindbis viruses from mosquitoes collected in the Nile valley of Egypt during an outbreak of Rift Valley fever. J Med Entomology. 2002;39:248–250. [PubMed] [Google Scholar]
- Morsy T, Fayad ME, Salama MMI, et al. Some myiasis producers in Cairo and Gaza abattoirs. J Egyptian Club Parasitology. 1991;21:539–546. [PubMed] [Google Scholar]
- Sabin AB, Blumberg RW. Human being infection with Rift Valley fever virus and immunity twelve years later on unmarried attack. Proc Soc Exper Biol Med. 1947;64:385–389. [PubMed] [Google Scholar]
- Ben-Nathan D, Lustig S, Tam Thousand, et al. Prophylactic and therapeutic efficacy of human intravenous immunoglobulin in treating W Nile virus infection in mice. J Infect Dis. 2003;188:five–12. [PubMed] [Google Scholar]
- Imam IZE, Karamany RE, Darwish MA. Epidemic of Rift Valley fever (RVF) in Egypt. I: isolation of RVF virus from animals. J Egypt Public Health Assoc. 1978;53:265–268. [PubMed] [Google Scholar]
- Taylor RM, Piece of work TH, Hurlbut HS, et al. A study of the ecology of Westward Nile virus in Arab republic of egypt. Amer J Trop Med Hyg. 1956;5:579–620. [PubMed] [Google Scholar]
- Salem HH. Myiasis in Arab republic of egypt. J Egypt Med Assn. 1935;18:238–246. [Google Scholar]
- Omar MS, Abdalla RE. Cutaneous myiasis caused by tumbu fly larvae, Cordylobia anthropophaga in southwestern Saudi arabia. Trop Med Parasitol. 1992;43:128–129. [PubMed] [Google Scholar]
- Edungbola LD. Cutaneous myiasis due to tumbu-wing, Cordylobia anthropophaga, in Ilorin, Kwara State, Nigeria. Acta Tropica. 1982;39:355–362. [PubMed] [Google Scholar]
- Shohami D. Israel storm chasing and weather condition photography — 2002-2003 picture gallery. 21 February-16 May 2003 [Internet] [cited 16 May 2003]. Bachelor from: http://wx0203.netfirms.com/02-03/storm0203-two.html.
- BBC News. Earth wonders at heaven'south gift [Internet] [cited 24 Baronial 1999]. Available from: http://news.bbc.co.uk/i/hi/sci/tech/specials/total_eclipse/417694.stm.
- Baron S. The Desert Locust. New York: Charles Scribner's Sons; 1972. pp. 97–153. [Google Scholar]
- Forum for Evolution and Man Rights Dialogue. January 2006 witnessed 97 accidents, 127 bodies and 567 injured road accidents: a violation to the right to life in Arab republic of egypt [Internet] [cited 12 February 2006]. Available from: http://www.moltaka.org/en/problems/06/0212.html.
- Turell MJ, Rossi CA, Bailey CL. Issue of extrinsic temperature on the ability of Aedes taeniorhychus and Culex pipiens to transmit Rift Valley fever virus. Amer J Trop Med & Hyg. 1985;34:1221–1228. [PubMed] [Google Scholar]
- Dohm DJ, O'Guinn ML, Turell MJ. Consequence of ecology temperature on the ability of Culex pipiens (Diptera: culicidae) to transmit West Nile virus. J Med Entomol. 2002;39:221–225. [PubMed] [Google Scholar]
- Fromkin H, Hess J, Luber G, et al. Climate change: the public health response. Amer J Public Wellness. 2008;98:435–445. [PMC free article] [PubMed] [Google Scholar]
- Salazar P, Traub-Dargatz JL, Morley PS, et al. Issue of equids with clinical signs of West Nile virus infection and factors associated with death. J Amer Veter Med Assn. 2004;225:267–274. [PubMed] [Google Scholar]
- Woods OL, Meegan JM, Morrill JC, et al. Rift Valley fever virus. In: Zinter Z, Morein B, editors. Virus Infections of Ruminants. New York: Elsevier; 1990. pp. 481–494. [Google Scholar]
- Easterday BC, Murphy LC, Bennett DG. Experimental Rift Valley fever in lambs and sheep. Am J Vet Res. 1962;23:1231–1240. [Google Scholar]
- Scott GR, Coackley Westward, Roach RW, et al. Rift Valley fever in camels. J Path Bact. 1963;86:229–230. [PubMed] [Google Scholar]
- Imam IZE, El-Karamany RE, Darwish MA. Epidemic of Rift Valley fever in Egypt. J Arab republic of egypt Public Health Assoc. 1978;53:265–268. [PubMed] [Google Scholar]
- Ali AM, Kamel S. Epidemiology of Rift Valley fever in domestic animals in Arab republic of egypt. J Egypt Public Health Assoc. 1978;53:255–259. [PubMed] [Google Scholar]
- Federation of American Scientists. Rift Valley fever: commencement out of Africa [Internet] [cited 16 January 2001]. Available from: http://www.fas.org/ahead/disease/rvf/outbreak/2000arabia.htm.
- Grandin T. Cess of stress during handling and transport [Internet] In: O'Driscoll J, editor. Information Resource for Livestock and Poultry Handling and Ship. Beltsville, Maryland: United States Department of Agriculture, Animal Welfare Center; [cited 27 April 1999]. Available from: http://www.nal.usda.gov/awic/pubs/livestock/lvstfull.htm#toc5. [Google Scholar]
- Ben-Nathan D, Lustig S, Feuerstein Yard. The influence of common cold or isolation stress on neuroinvasiveness and virulence of an adulterate variant of Due west Nile virus. Arch Virol. 1989;109:1–10. [PubMed] [Google Scholar]
- Al-Hazmi G, Ayoola EA, Abdurahman M, et al. Epidemic Rift Valley fever in Saudi arabia: a clinical report of severe illness in humans. Clin Infec Dis. 2003;36:245–252. [PubMed] [Google Scholar]
- Wilson ML, Chapman LE, Hall DB, et al. Rift Valley fever in rural northern Senegal: human risk factors and potential vectors. Am J Trop Med Hyg. 1994;50:663–675. [PubMed] [Google Scholar]
- Nabeth P, Kane Y, Abdalahi MO, et al. Rift Valley fever outbreak, Islamic republic of mauritania, 1988: seroepidemiologic, virologic, entomologic and zoological Investigations [Internet] [cited 15 Dec 2006]; Emerg Infect Diseases. Available from: www.cdc.gov/ncidod/EID/vol7no6/nabeth.htm. [Google Scholar]
- Georges AJ, Lesbordes JL, George-Courbot MC, et al. Fatal hepatitis from Westward Nile virus. Ann Institut Pasteur/Virology. 1987;138:237–244. [Google Scholar]
- Mathiot CC, Georges AJ, Deubel V. Comparative analyses of West Nile virus strains isolated from human and animal hosts using monoclonal antibodies and cDNA restriction digest profiles. Res Virol. 1990;141:533–543. [PubMed] [Google Scholar]
- Yassin W. Clinico-pathological motion-picture show in five human cases died with Rift Valley fever. J Egypt Public Health Assoc. 1978;53:191–193. [PubMed] [Google Scholar]
- Ruffer MA. Notes on the presence of "Bilharzia Haemotobia" in Egyptian mummies of the Twentieth Dynasty (1250-1000 BC) Brit Med J. 1910;i:sixteen–25. [PMC gratuitous article] [PubMed] [Google Scholar]
- Glass WG, McDermott DH, Lim JK, et al. CCR5 deficiency increases risk of symptomatic West Nile virus infection. J Exp Med. 2006;203:35–40. [PMC gratuitous article] [PubMed] [Google Scholar]
- Ruiz MO, Tedesco C, McTighe TJ, et al. Environmental and social determinants of human risk during a West Nile virus outbreak in the greater Chicago surface area, 2002. [cited xv December 2006]; International J Wellness Geographics [Internet] 2004 three:eight. Available from: world wide web.ij-healthgeographics.com/content/3/1/8. [PMC complimentary article] [PubMed] [Google Scholar]
- Brownstein JS, Rosen H, Purdy D, et al. Spatial analysis of the Westward Nile virus: rapid risk assessment of an introduced vector borne-zoonosis. Vector Borne Zoonotic Dis. 2002;2:157–164. [PubMed] [Google Scholar]
- Arishi H, Ageel A, Abdu Rahman Chiliad, et al. Centers for Illness Command and Prevention. Update: outbreak of Rift Valley fever-Saudi Arabia, August-November 2000. MMWR. 2000;49:982–985. [PubMed] [Google Scholar]
- Dohm DJ, Turell MJ. Effect of incubation at overwintering temperatures on the replication of West Nile virus in New York Culex pipiens (Diptera: culicidae) J Med Entomology. 2001;38:462–464. [PubMed] [Google Scholar]
- Thompson DF, Malone JB, Harb Thousand, et al. Bancroftian filariasis distribution and diurnal temperature differences in the southern Nile delta. [cited 23 December 2007]; Emerg Infect Dis [Internet] 1996 2 Bachelor from: http://www.cdc.gov/ncidod/eid/vol2no3/thompson.htm. [PMC complimentary article] [PubMed] [Google Scholar]
- Hammon WMcD, Reeves WC. Summary and epidemiological correlations. In: Reeves WC, Hammon WMcD, editors. Epidemiology of the Arthropod-borne Viral Encephalitides in Kern County, California, 1943 -52. Volume four. Berkeley, California: University of California Press,University of California Publications in Public Health; 1962. pp. 178–217. [Google Scholar]
- Lancelot R, Gonzalez JP, Le Guenno B, et al. Epidemiologie descriptive de la Fievre de la Vallee du Rift chez les petits ruminants dans le sud de la Mauritanie après l'hivernage 1988. Revue Elev Med Vet Pays Trop. 1989;42:485–491. [PubMed] [Google Scholar]
- Gergis J, Braganza Grand, Fowler A, et al. Reconstructing El Nino-Southern Oscillation (ENSO) from high-resolution paleoarchives. J Quaternary Sci. 2006;21:707–722. [Google Scholar]
- Dewannieux M, Harper F, Richaud A, et al. Identification of an infectious progenitor for the multiple-copy HER-K human endogenous retroelements. [cited eleven December 2007]; Genome Res [Internet] 2006 16:1548–1556. Available from: http://www.genome.org/cgi/content/total/gr.5565706/DC1. [PMC free article] [PubMed] [Google Scholar]
- Mellor PS, Wittman EJ. Bluetongue virus in the Mediterranean basin 1998-2001. Vet J. 2002;164:xx–37. [PubMed] [Google Scholar]
- Rezza G, Nicoletti L, Angelini R, et al. Infection with chikungunya virus in Italia: an outbreak in a temperate region. Lancet. 2007;370:1840–1846. [PubMed] [Google Scholar]
- Asnis D, Conetta R, Waldman G, et al. Centers for Disease Control and Prevention. Outbreak of West Nile-like viral encephalitis — New York, 1999. MMWR. 1999;48:845–849. [PubMed] [Google Scholar]
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2442724/
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