Part 2 of 3
Brad Sparks
Hort’s Twelve Fatal Scientific Errors
Scientific errors in the Hort theory of the Ten Plagues of Egypt are glaring (Sparks 2003). Hort’s postulated blanket of thick red Nile silt was so dark she claims it caused the pitch-lack Plague of Darkness, when blown into the air. It never occurred to Hort that it would first cause an underwater Plague of Darkness. Before the silt ever got into the air it would have done the same thing in the water, blacking out the sunlight needed for photosynthesis by the algae, thus killing the algae outright. Hort cannot have both her silt and her algae at the same time.
Likewise, by requiring that the algae plague take place during the flood season Hort self-destructs her own theory, as it is the one time of the year when field studies prove that—due to the silt blotting out the sun and other algae-destroying effects—the Nile is completed clear of algae. It is quite unfortunate that Hort did not do the basic research to uncover this fundamental fact of Nile biology. The other major algae-killing property of Nile silt is flocculation, the process of mud particles sticking to algae and sinking, and there are still several additional Nilotic effects that kill algae as well. Because Hort’s theory requires both the algae and the silt that kills the algae, her theory is logically and scientifically self-destructing.
Many of Hort’s errors rise to the level of fatal flaws, entirely disproving her thesis, and the rest certainly shake, if not shatter, our confidence in the quality and reliability of her investigation. It takes only one broken link to destroy the chain of scientific evidence for a theory. Here there are at least 12 fatal scientific blunders by Hort. In each case the basic information on the Nile or the general scientific principles was known or available as of 1957–1958 when Hort published her paper:
1. Season Wrong.
2. Algae-Killing Nile—No sunlight, No Photosynthesis, No Algae.
3. Algae-Killing Nile—Algae Stick to Silt (Death by Flocculation).
4. Silt Color Wrong—Brown not Red.
5. Habitat Wrong—Hort Algae Never Found in Nile.
6. Algae Color Wrong—Green not Red.
7. Harmless Hort Algae—Non-Toxic, Non-Polluting.
8. Red Tides in Oceans, not Rivers.
9. No Fish Kills.
10. Algae-Killing Nile—Destructive Physical Force.
11. Algae-Killing Nile—Turbulence Disrupts Stagnant Algae.
12. Algae-Killing Nile—Fatal Habitat Changes Down River.
Hort’s Microbiology Errors
Hort’s major microbiology error include:
• Photosynthesis: Omitting the fact that plant algae need sunlight to grow, and that sunlight would be absent in heavy Nile silt.
• Algae Color Classification: Mistaking the color of the culprit green algae as red.
• Habitat: Ignoring the recorded habitats of her algae, which are actually used as “industrial indicators” of snow and ice water below 5° C (41° F) (Palmer 1980:72, table 23; Yuan and Chen 2000). Obviously they are neither tropical or riverine, nor ever reported from the Nile. The algae are rare and so non-robust they can barely survive (Pringsheim 1966:1–2, 5). Anthrax doesn’t multiply in rivers and doesn’t infect aquatic life.
• Field Studies: Insisting against the scientific-historical evidence that algae “would appear only at a time when the Nile was at its highest” (Hort 1957:94, emphasis added), which is exactly opposite of the facts. It has never been proven that biting flies transmit anthrax.
Hort’s Geology Errors
Hort’s paper is filled with misinformation and fable, not “facts,” about the Nile’s geology, hydrology and climatology, all of which she employs to bolster her red tide theory of the Plagues. Her geology blunders include repeating the erroneous ancient Greek myth (Lloyd 1976:92–93, 101–102; Bonneau 1964:15; Wilkinson 1875:33 fn. 6: Rzóska 1976:145–53, 168–71, 225, 259–62, passim) that the Nile is fed by “melting snow” from the mountains of Ethiopia and that it is a major source of the Nile’s water (1957:88, 91; Hyatt 1980:336, 339, Cole 1973:91; Sarna 1991:38). She mistakes the color of the Nile flood sediments as red instead of brown. This demolishes her theory by eliminating one of her two absolutely crucial sources of red color in the water. She asserts the White Nile is white because of “decomposed vegetable matter” (1957:90), when the color is actually due to whitish volcanic sediment (Rzóska 1976:215). She claims the Blue Nile “really looks blue” and is “never” green (1957:90, 91)—when in fact it is green according to scientists who have spent their lives there and as is obvious in published photographs (Hammerton 1976:243: Rzóska 1976:263, 266–67 fig. 68). Hort has to suppress the fact of the green color because it is due to a different species of algae (Hammerton 1976:243) and obviously incompatible with her red algae theory. Hort never discusses the identify of any of the many species of algae actually living in the Blue Nile (or the main Nile for that matter, as mentioned in Part 1).
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View of the Nile Valley, looking north from the tombs at Beni Hasan in Middle Egypt.
Hort’s Climatology Errors
Hort fails to consider that in the wetter climate of the past the Nile water level was much higher, carrying a larger volume of water. Thus it was much more inhospitable to algae growth than it is today, heavy torrents being the total opposite of stagnation. It may well be that the Nile could not sustain any significant bloom of algae at the time of the Ten Plagues, whether a harmful red tide or not. Climatological evidence shows that overall there has been a strong drying trend from the Neolithic era to classical times that has lowered the Nile (Butzer 1976:28–33; Butzer 1984; 107; Hassan 1997; Claussen, et al. 1999).
Hort makes questionable changes in the Hebrew text of Exodus so that the west wind that blows the locusts back into the Red Sea becomes a north wind or sea wind. She also changes the east wind that brings the locusts into a south wind, because the locusts are supposed to come from the Sudan or southwestern Arabia, which are south or southeast of Egypt (1958:49–52).
Hort suggest the Plagues of Hail and Darkness were naturally restricted to Southern Egypt and so avoided the Israelites in the Nile Delta of northern Egypt. She claims that hailstorms only occur in the North in April-October (partially incorrect in any case; De Vaux 1978:361 fn. 5; contra Hort 1958:48–49), hence a February Plague of Hail could only occur in southern Egypt, but presents no evidence that hailstorms ever naturally occur in February anywhere in Egypt. Hort inconsistently insists that the hailstorm added moisture yet the earth was dry enough for the silt dust to create the darkness.
Hort’s theory about the Plague of Darkness switches from the usual khamsin sandstorm that raises sand from the desert, to one that raises dust from the Nile banks from supposedly dry river sediment. This makes for insuperable difficulties, such as how the river banks could possibly have turned dry so suddenly by natural processes in a logical order, as Hort claims, when she also asserts it was an “unusually wet winter” with such “widespread flooding of the country” that it left the land “waterlogged for longer than usual” (at least two to three weeks longer: 1957:100, 1958:49–50, emphasis added). What happened to all the excess water the Egyptians reserved for agriculture later in the year? If the Hailstorm Plague of “quite unusual violence” was wet with an additional “pelting rain” as Hort claims (1958:49), contrary to the Bible how could the earth dry so fast in the few weeks from early February to early March (in her timetable), in the midst of this “unusually wet winter”?
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But the time available for the country to dry out is much tighter than even this: Hort needs the land of the Nile unusually wet so that anthrax germs, frogs, mosquitoes, flies and locusts can breed or hatch at a tremendous rate. Then she inconsistently needs the land to be unusually dry so soil can be blown aloft in an excessively dark dust storm. She leaves very little time in between, from the Locust Plague, probably during most or all of February, until the Plague of Darkness in early March (in her timetable), to go from crop destruction to dustbowl, with nothing to cause a sudden mid-winter weather change other than the Khamsin sandstorm, which would have to carry out this drying in the brief “two to three days” that Hort admits it generally involves (1958:53). But the timing is even tighter still: The Plague of Darkness lasts three days. The Khamsin that supposedly causes the darkness by blowing the dried Nile silt into the air also lasts three days at most. That leaves at best a fraction of the first day, or just hours, for the khamsin to successfully dry out the entire Nile valley and raise the dust to cause the Plague of Darkness over essentially three days. How such a khamsin could dry the soil with what must have been an unusually high water table underneath due to the extremely high flood and wet winter is even harder to fathom.
Crops normally have “little or no need for further watering,” even up to ripening in March-April, because the ground stays moist. It is only after the harvest that the ground dries and cracks, in the summer (Kemp 1989:10: Butzer 1976:17 Willcocks and Craig 1913:304; White 1970:2) before the next flood has overflowed the banks. In an “unusually wet” year as postulated by Hort this moistness would persist even longer (she suggests at least two-three weeks longer), or well past April harvest and into May, and thus well after the Plague of Darkness dated by Hort to early March. It is buffing that Hort could not see that her high-flood-wet-winter scenario creates a gross discrepancy of timing of at least two months in her timetable of Plagues.
Hort’s Epidemiology Errors—Anthrax and Flies
Hort claims the Second, Fifth and Sixth Plagues were caused by anthrax, with the last one spread by the Stomoxys calcitrans biting stable fly. But biting stable flies have never been medically or epidemiologically documented to spread anthrax to cattle or humans, and they do not feed on dead animals. Scientists in East Africa mention this fly species, but no outbreaks of anthrax are found in the mass of medical entomology and veterinary data studied (Rzóska and Lewis 1976:208, 330–31). Occasional attacks of Stomoxys flies such as in 1962 and 2001 have occurred in small areas of Tanzania after heavy rains, but against animals not humans, not near the Nile or its sources, and not with any anthrax outbreaks (Arusha Times 2001; Discovery News 2001; Reuters 2001). Hort claims these biting stable flies hatched and spread the Plague of Boils in early January, but they would have been in the hibernating pupa stage in the winter (Nass 1992; Cunha 2002; ECORC2001;USDA 2001).
A natural phenomenon must naturally occur. Yet there is no natural occurrence in the Nile valley of this purported natural phenomenon of an insect carrying anthrax—of any insect, let alone the Stomoxys fly, which is so crucial to Hort. Eleven diseases carried by insect vectors are mentioned in East Africa, but not anthrax. In fact, anthrax spread by any means is sufficiently rare in Egypt that it is only sporadically reported in the medical literature (WHO CC 2000).
Hort’s Frog Plague theory of anthrax killing the frogs after they invaded the Egyptians’ homes is contradicted by basic epidemiology, as anthrax cannot infect frogs. (Marr and Malloy 1996:12–13, 15). Anthrax only infects mammals, typically grazing herbivores such as sheep, cattle and goats, and does not infect frogs, amphibians, reptiles or fish (USDA 2001:AVMA 2001;Cunha 2001: UN FAO 2001). Thus Hort’s fish could not contract anthrax either. Anthrax is a soil contaminant and is not contracted from large bodies of water such as rivers. Hence, even if the fish could develop anthrax they would never encounter any anthrax in the Nile in the First place.
According to the Centers for Disease Control and Prevention (CDC) in Atlanta, anthrax disease comes in three forms by site of infection (CDC 2001): (1) Skin (cutaneous), (2) Inhalational (pulmonary or lung), or (3) Gastrointestinal (internal). These are not different strains. The same organism causes each, differing only as to where the bacteria lands on the body and succeeds in developing an infection. Skin anthrax infections in humans are about 20% fatal if untreated, though nearly 100% fatal to animals, and these would be approximately the mortality rates in ancient Egypt at the time of the Exodus (cf. Marr and Malloy 1996:15). As recent events have shown, it is the rare inhalational anthrax that is most virulent and nearly 100% fatal, rather than the more common skin anthrax, contrary to Hort. The terrorist-induced inhalational anthrax cases require large amounts of highly purified weaponized anthrax, which would never occur in nature.
Anthrax is a disease that mainly affects livestock animal such as sheep and cattle in agricultural regions, especially in the Third World, including the Middle East, but also in industrial nations that process cattle hides, leather and wool. It is caused by a rod- shaped bacterium found in the soil, Bacillus anthracis, that forms a tough dry covering or spore when exposed to air. The anthrax spore can survive for long periods of up to 80 years or more under harsh conditions, a feature that has made it of special interest to designers of biological weapons. The egg-shaped spores is lifeless until it comes into contract with an animal or human. Then it bores into a white blood cell, multiplies, bursts the cell and spreads to other white blood cells and lymph nodes, attacking the immune system to repeat the process, like a bacterial version of the AIDS virus HIV, only much more rapid. Victims develop fatal toxic shock from toxins emitted by the anthrax. Dead animals bleed into the soil where anthrax spores form and lie in wait for the next victims. The live or “vegetative” anthrax bacilli are fragile and won’t survive 24 hours outside an infected animal or human host unless turned into dry spores (Inglesby 1999; New Scientist 2002; Bowen 2001; Holmes 2001). Anthrax was named after the Greek word for coal, anthrakis, because of the black lesions formed on the skin.
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The Plague of Frogs. “So Aaron stretched out his hand over the waters of Egypt, and the frogs came up and covered the land…And the Lord did what Moses asked. The frogs died in the houses, in the courtyards and in the fields. They were piled into heaps, and the land reeked of them” (Ex 8:6, 13–14).
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The main way anthrax is transmitted to humans is by direct contact with infected meat or hides and wool through cuts or abrasions in the skin; hence it is very infectious (some authorities flatly state it is “not contagious”: UN FAO 2001). Animals contract the disease mainly by grazing on grass contaminated by anthrax spores in the soil. Wild carnivores may get anthrax by eating infected meat or carcasses in rare cases. Neither mode of transmission is invoked by Hort. Anrthrax bacilli typically attack the blood of sheep. Thus Hort’s theory of widespread anthrax contamination and disease in Egypt, including among sheep, would turn the Passover ritual into a deadly act of mass exposure to anthrax-infected lamb meat and blood. This would have triggered a runaway anthrax epidemic focused on the Israelites instead of the Egyptians, again tripping up Hort’s claim to scientifically show how “natural” Plagues would have avoided the Israelites.
According to the CDC, “anthrax has an inability to penetrate intact skin” (Cieslak and Eitzen 1999). How could large numbers of Egyptians (and their animals with tough hides) have such breaks and then get anthrax infections specifically in those breaks?
Hort’s ingenious theory of anthrax transmission is to break the skin and hide with supposedly anthrax-laced bites from the East African biting stable flies—even though it is a physical impossibility for the flies to bite through tough animal hides. This novel idea is undocumented in the medical-veterinary history of anthrax, with no known cases of anthrax-infected fly bites of humans, cattle or sheep anywhere in the world (Rzóska and Lewis 1976; Nass 1992; Cunha 2002). Biting stable flies bite live animals and do not feed on carcasses. Hence Hort’s theory cannot get the anthrax from the dead animals in the Fifth Plague to the live animals and humans in the Sixth Plague with these flies.
Experiments have so far failed to coax Hort’s biting stable flies into transmitting anthrax to large ruminants with tough hides or thick wool, even under contrived and forced conditions that would never occur in nature, such as requiring that flies carry huge impossible does of more than 600 million anthrax spores in order to infect one cow. Only with great difficulty under forced conditions have such flies passed anthrax to small mice and guinea pigs that only requires 5 to 50 spores to infect, and still only a 12–17 percent transmission rate was achieved. Nile and East African biologists and epidemiologist have never seen such fly-vector anthrax cases in cattle or humans (Nass 1992; Rzóska and Lewis 1976; USDA 2001).
Typically anthrax outbreaks occur during droughts or after floods (USDA 2001; UN FAO 2001). Anthrax collects on plants and in soil, not in engorged rivers where the bacteria are thoroughly diluted. Flooding overturns and exposes anthrax-contaminated soil and causes fresh grass to grow in it. The animals eat this anthrax-laced grass and develop gastrointestinal anthrax. But Hort has the supposedly anthrax-driven frog frenzy take place in August, during, rather than after, the annual Nile flood, as the river is reaching its highest levels, when any anthrax would be diluted the most, not the least. This makes no sense. Droughts force grazing livestock to eat closer to the ground, so they could ingest more soil with anthrax spores. But that does not help either, as Hort’s ultra-high floods are opposite of drought. The last resort might be Hort’s theory of the khamsin winds drying out the land. But these But these winds occur in March, seven months too late for Hort’s scenario to work. In reality, Hort’s ultra-high Nile flood self-destructs her theory here once again because the extraordinary waterlogging of the land of Egypt (much more than the ordinary annual flooding) would wash away anthrax, prevent anthrax bacilli from collecting in sufficient number to cause infection, and would also prevent the khamsin winds from drying out the land for an extended period.
If anthrax had infected a large proportion of the Egypitan population of a few million, as Hort contends, then such a natural occurrence would recur again sometime in history. Known areas susceptible to anthrax in other parts of the world have long histories of outbreaks, because anthrax spores remain in the soil for centuries and disease outbreaks rarely spread to new areas. But Egypt has no notable anthrax history (WHO 2000). Natural outbreaks that do occur anywhere in the world are rare and not very large—these plagues are not of “Biblical” proportions. The largest known recorded anthrax outbreak in history occurred in Zimbabwe in Southern Africa in 1978–1980 with 10,738 human cases reported. But biowarfare is suspected and there was no evidence of biting flies (Nass 1992; Friedlander 1997).
The anthrax theory of the Plagues dates back well before Hort to Henry Blanc. In 1890 Blanc, writing in an obscure medical journal, suggested that anthrax killed the frogs, was transmitted by flies to animals and humans, and even caused the Plague of the Firstborn. Epidemiologist john Marr rejects the anthrax etiology of the middle Plagues because the relatively high death rate for skin anthrax, of approximately 5–20 percent for humans, would have been noticed and commented on in the Bible. Marr contends that such large death tolls only occurred at the very end with the Plague of the Firstborn, where he estimates the death rate at about 10 percent, and that these mass deaths were, of course, well noted (Marr and Malloy 1996:18, citing Blanc 1890).
Critiques of Other Naturalistic Theories of the Plagues
Greta Hort has succeeded so well in packaging her red algae theory of the Ten Plagues of Egypt as a “scientific” theory, that it has escaped scientific criticism, paradoxically. Despite the numerous glaring errors and self-destructing contradictions in Hort’s red algae and red silt theory of the Ten Plagues (e.g., the river silt kills the algae), no detailed scientific, literary or historical criticism of Hort’s work has ever been published, until now.
The main criticism occasionally aired against Hort and against naturalistic theories of the Plagues in general has been that if they were truly a natural occurrence they should have naturally occurred again and again, and not just once in the time of Moses. But nothing like the Plagues has ever occurred again (Sarna 1986:75; De Vries 1975:1349–50; Salkeld 1995). Natural occurrences would not be new to the Pharaoh and would “not have impressed the Egyptians.” Only “something unusual” would have (De Vaux 1978:360–64; De Vries 1975: ibid.; Hill and Walton 1991:114–15, 2000:114–15; cf. Bechtel 1911). If extreme circumstances were required for the Plagues to occur naturally—e.g., Hort’s theory that excessive annual Nile flooding unleashed a torrent of red algae and red mud—then, when those extremes were repeated through history, at least a partial set of Plagues should have occurred again. The Nile flooded excessively in 1359–1360 and 1817, for example, yet not even a partial set of Plagues occurred then—no “blood plague,” no water pollution, no “plagues” at all (Salkeld 1995; cf. Sarna 1986:75).
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The unexplained exemption of Goshen from the Plagues and the selectivity of the Plague on the firstborn have also been said to be clearly unnatural (Hill and Walton 1991, 2000, ibid.; Bechtel 1911). Some seem to accept Hort’s work for the first nine Plagues only, excluding “of course,” the last Plague, “which is meant to represent God’s triumph over Pharaoh,” as one Egyptologist put it (Lesko 2000).
Attempts to explain the supernatural miracles of the Plagues as natural occurrences date back to Benedict de Spinoza in 1670. Successors in seeing the Plagues as natural phenomena include Thomas Morgan (1737), Leonhard Bertholdt (1795). Aimé du Bois-Aymé (1809:291–324), Johann Eichhorn (1818) and Peter von Bohlen (1835:56). In 1794 English mythologist Jacob Bryant may have been the first to argue against a naturalistic Ten Plagues theory, when he estimated the date of the Plague of Blood as January or February and argued that the naturalistic explanation is contradicted by the fact the Nile water is still “particularly pure and wholesome” at that time of year (Bryant 1810:79–84).
Travelers to Egypt in centuries past have sometimes tried to account for the Blood Plague as a “natural phenomena of Egypt,” such as an especially severe instance of supposedly “red” mud of the Nile in its annual rising midsummer flood (Henstenberg 1843:106–107, quoting traveler Sonnini for example), though the Nile is actually brown—not red—when silt-laden, as has been discussed earlier. But if there merely had been mud of whatever color in the water, the Egyptians had several standard methods for clearing the mud from the water. As Hengstenberg noted, the most common method was to simply let the water stand in vessels until the mud settled to the bottom, which they normally did in order to drink it (Hengstenberg 1843:110, alluding to Hartmann 1791:130, 1799; Helffrich 1580). If they were in a hurry, faster method included straining the mud out through earthen jars with many tiny holes (minutis foraminibus Plenae) or using almond paste or a special white-earth filter.
The Plague of Flies. “Dense swarms of flies poured into Pharaoh’s palace and into the houses of his officials, and throughout Egypt the land was ruined by the flies” (Ex 8:24).
Some 19th century commentaries mistakenly recite that pioneering biologist Christian Ehrenberg thought the Blood Plague was due to the supposed natural redness of the Nile caused by “cryptogams and infusoria” (algae and protozoan) and “red earth” (Cook 1871:277, citing a commentary by Carl F. Keil and Franz Delitzsch on Ex 7; Lange 1876:20). But the actual 1830 paper by Ehrenberg only mentions reddish algae stains on dry salt beds and in a stagnant pond, not in the Nile itself, and does not even mention the Blood Plague (Ehrenberg 1830).
The first modern scientific study of algae in the Nile or its sourced did not occur until 1888, 50 years after Ehrenberg, and was conducted by Franz Stuhlmann and Emin Pasha at Lake Victoria (Rzóska 1976:335, 405).
Hort herself rejects German critic August Dillmann’s 1897 explanation of the red color of the water as due to algae and dust because it accounts only for the stench of the water and supposedly not the exact “blood-red” color, which she claims sole credit in explaining (1957:88, 93–94, citing Dillmann 1897).
Some more recent proposals for explaining the Plagues biologically have been critiqued by Marr and may be dismissed for the same reasons previously covered in the present paper (Marr and Malloy 1996:10, 14–16, 18–20). Regina Schoental (1980) has suggested that fungus contaminated the water in the Blood Plague, but that dinoflagellate algae killed the frogs, then mycotoxins struck in the middle and final Plagues. Needless to say, no such Red Fungus Nile is known to science, H. M. D. Hoyte of Australia (1993) and Giovanni Ceccarelli fo Italy (1994) have proposed that dinoflagellate algae of the common Gymnodinium and Glenodinium genuses caused the Plague of Blood. But dinoflagellate red tides occur in the ocean, not in freshwater rivers. All these algae suggestions run into the same problems with the algae-killing properties of a major freshwater river such as the Nile, as already cited. As previously discussed in Part 1, mycotoxins do not explain the circumstances of the last Plague, M. G. Jacoby (1983) and Ludwig Schmidt of Germany (1990) suggest that the Nile became undrinkable merely by contamination from the dead fish, avoiding the role of the blood pollution of the Nile in the Biblical account (Ex 7:17–20), but not explaining what killed the fish.
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Hort’s Domino Theory
Hort asserts the following schedule of Plagues, similar to Macalister’s 1902 scheme, which she does not mention. She presumptuously declares some dates as not just “accurately fixed,” but as fixed with “absolute certainty” (1957:99:1958:49, emphasis added):
* 1. July of August:
First Plague—Blood. Extremely heavy rains and “snow” at the headwaters of the Nile scour tremendous loads of “Roterde” (red earth) from gorges in the Abyssinian Plateau. Red algae make the river even redder and kill the fish in it, giving rise to a foul stench (Hort 1957:88–95).
* 2. August:
Second Plague—Frogs. Dead fish give rise to anthrax bacteria, which sicken the frogs, driving them ashore, only to die in great numbers at almost the same time (Hort 1957:95–98).
* 3. October-November:
Third Plague—Gnats or Lice. Mosquitoes bread under the unusually high Nile flood (Hort 1957:98–99).
* 4. Late Dec/early Jan:
Fourth Plague—Flies. Biting stable fly Stonroxys calcitrans also breeds tremendously in the decaying plant debris left by the excessive Nile flood (Hort 1957:99, 102–103).
* 5. Early January:
Fifth Plague—Animal Disease. “Internal anthrax” later infects the cattle and other livestock (Hort 1957:100–101).
* 6. Late Dec/early Jan:
Sixth Plague—Boils. Fly Stomoxys calcitrans is a carrier of anthrax bacteria with its bite causing a “skin anthrax” of severe boils on both man and animals (Hort 1957:102–103).
* 7. Early February:
Seventh Plague—Hail and Fire: Hailstorm strikes the southern Egyptian valley of the Nile, missing the Israelites in the north, with its Mediterranean climate zone (occasional storms there only from April to October). Flax and barley were not at a stage to be destroyed by hail except in January or February (Hort 1958:48–49).
* 8. February:
Eighth Plague—Locusts. Unusually wet winter with its high Nile flooding also breeds mass swarms of locusts (Hort 1958:49–52).
* 9. Early March:
Ninth Plague—Darkness. Extraordinarily deep deposit of extremely fine red earth left from the First Plague has now dried and is kicked up into the air by the first khamsin desert sandstorm of the year, which blots out the sun (Hort 1958:52–54).
* 10. March/April:
Tenth Plague—Harvest “First fruits” not “Firstborn” Children. It is not the death of the firstborn children but the destruction of the last remains of the firstfruits of the harvest that is meant here, due to a corruption in the Bible text (Hort 1958:54–55).
There is no hard evidence given that requires this exact eight-nine-month schedule, much of which is actually quite arbitrary or erroneous when investigated in depth (see earlier discussion). Many other timetables of the Ten Plagues, equally as arbitrary and conflicting with Hort’s, have been devised by scholars ranging in total length from as little as one month to as long as one year (see, e.g. Humphreys 2003:144–45, where half of the Plague dates disagree with Hort’s by a month or more).
Hort contends that “the primary clue which we have to the nature of the first plague” is “the intensity of the redness being so great as to make the Nile water look like blood” (1957:87, emphasis added). Hort does not explain why the intense blood-red color must be the one single “primary clue.” She rather arbitrarily lists the following as the secondary of “attendant” phenomena reported in the Bible, again without and scientific or other explanation why these are relegated to lower importance: (1) The spread of the blood-red water throughout Egypt; (2) death of the fish in the Nile; (3) the stench of the Nile; (4) the undrinkability or impotability of the Nile water; and (5) the fact that “all” Egyptian had to dig around the river for water to drink.
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The Plague on Livestock. “And the next day the Lord did it: All the livestock of the Egyptians died, but not one animal belonging to the Israelites died” (Ex 9:6)
Red-colored algae are absolutely essential to Hort’s theory. She severely criticizes red-mud-only theories as totally inadequate to account for the deep “blood-red” color of the Nile. There must be “mass” amounts of red-colored algae to redden the river and kill the fish—mere mud of any color in the Nile would not kill fish or cause a stink, Hort argues (1957:94, emphasis added: “mass of flagellates”; “mass appearance”). Yet Hort also rejects Dillmann’s theory even though it included both red algae and soil, just because he did not make the argument of red algae enhancing the color of the red mud to make a “blood red” color (1957:88, 93–94, citing Dillmann 1897). This fine hairsplitting argument, of course, is a convenient rationalization to distinguish predecessors’ theories from Hort’s and to dismiss them as inadequate, so as to preserve her right to claim priority of discovery. But, as we have seen, there is no scientific substance to Hort’s theory—no red algae, no red mud, and no red color at all to argue about in the first place.
Can We Salvage Hort’s Theory?
As noted earlier, any attempt to save Hort’s theory by fixing its numerous scientific errors would utterly overthrow her scheme and create a different set of insuperable problems—”saving” her theory merely destroys her theory. Hypotheszing the remote possibility of a Green Toxic Nile as a “natural phenomenon” would be one that mainly attacks the Israelites instead of sheltering them. If we pursue such an idea despite this egregious difficulty, a surprise mass algae bloom might have been triggered by the sewage runoff from the large slave population, abruptly appearing and rapidly expanding in the Eastern Nile Delta over the course of several decades leading up the time of the Exodus. An increase in the number and severity of Harmful Algal Blooms has been noticed along coastlines and estuaries of several regions of rapid population growth from the 1950s to date (e.g., Long Island “green tide” of the 1950s, Mississippi river efflux into the Gulf of Mexico 1950s, Seto Inland Sea of Japan 1965–85. Hong Kong’s Tolo Harbor 1976–86. Pfiesteria outbreaks in North Carolina and Maryland in the 1980s and 1990s). Some scientists have suggested that the nutrient enrichment (eutrophication) of coastal waters from the increased water pollution (agricultural runoff and waste water) in these populated areas has stimulated overgrowth of algae. This interpretation is not certain and has been disputed, based on a number of counterexamples not attributable to such eutrophication, such as the toxic red tides or HAB’s in southern New England in 1972, North Carolina in 1987, and West Coast U.S. in 1991 (NOAA 1999:7: NSTC 2000:12–14, 22, 23).
This attempted hypothetical rescue of Hort’s theory ignores the much greater volume of the Nile in the past, with its much greater algae-killing effects, as well as its outright dilution of sewage runoff. It ignores the fact that the Delta region is purely freshwater (oligohaline), not saline, whereas the eutropbhication effect in producing HAB’s is seen in salt water (cf. Marr and Malloy 1996:10). Such HAB’s would be concentrated in the Israelite areas rather than the Egyptian areas, just the opposite of the result sought by Hort. She advertises as one of the great selling points of her theory a “natural” avoidance of the Israelites that is supposed to scientifically explain the impression in the Book of Exodus that the Israelites were miraculously sheltered from some, if not all, of the Plagues.
Of course this attempt to help fix Hort’s theory has the advantage that it does not use her nonexistent algae from the East African lake, but generates the algae locally from real Nile algae (if it is possible at all), and tries to employ a novel biological speculation that has some scientific basis, instead of Hort’s that has no basis at all.
But, alas, most of the remaining objections to Hort’s theory also apply to this alternative Green Nile scenario (wrong color, many algae-killing effects o f Nile silt, lack of red tides in rivers, lack of red algae blooms ever found in Nile waters, etc.).
BSpade 17:1 (Winter 2004) p. 25
Notes
1 Though, Bell prefers to see the drying trend ending with Nile levels as reaching modern levels in the Middle Kingdom or later (as Butzer shows), she nevertheless does refer inconsistently to a “return of the Nile to generous floods” in the Middle Kingdom’s 12th Dynasty which would mean lower levels followed later (Bell 1975:224). Butzer’s paper incorporates more recent data and reports evidence of a continuing drying pattern of the Nile levels into the New Kingdom period and beyond. Nile levels are not to be confused with regional climatic conditions, which are more complex (see Butzer 1976:33, 51 [“long term trends of decreasing flood volume” in Dynastic period], 52, fn. 6; Butzer 1984:107–108, 109–10, 111, passim).
2 Hort suggest the Locust Plague occupied most or all of February when she states “we are now in the month of February” and that locusts typically invade Egypt and Palestine from “March till the beginning of May,” which indicates a duration of locust infestation of at least two months (1958:50, emphasis added).
3 Sleeping sickness, yellow fever, malaria, oriental sore, kalaazar, sand fly fever, schistosomiasis trypanosoiasis (affecting animals), human loiasis, allergies and asthma (Rzoska, Thompson and Lewis 1976:74, 190, 208, 325–31, 346–50).
4 Cited in Childs 1974:167; Hengstenberg 1843:96–97. See Elwes 1955:91, cited in Brown 1984:30–33, 331, n. 22; see Baumer 1960:89. Hengstenberg mentions that Reformation theologian John Calvin “hints” at a “connection of the supernatural with the natural” in his commentary on the Plague of Frogs (Hengstenberg 1843:99 fn.).
5 Murray 1914:132; see Hengstenberg 1843:110–11; Suidas on Kanpopos,” cited in Bryant 1775:248 and fn. 49; 1807:71–72 and fn. 49, also citing Ruffinus, Ecclesiastical History, book 11, ch. 26. See also Macalister 1902:889, partly citing: Alpinus 1591:16: Norden 1757:52; Sonnini 1799:124; von Troilo 1677:472; Volney 1788:20; Galen 1543:3, sec. 2.
6 Niebuhr 1792:71–72; hengstenberg 1843:110–11, partly citing: Prosper Alpinus who wrote on the plants, medicines and natural history of Egypt (Alpinus 1591, 1592, 1735); Pococke 1773:312, Savary 1786; Mayr 1820: sec. 19(?).
7 Hengstenberg 1843:110–11, partly citing: Bruyn 1714:103: Thevenot 1663:245, 60(?); see Bryant 1775:248 abd fbs, 48–49; 1807:71–72 and fns. 48–49.
8 Ehrenberg coincidentally identified and classified one of Hort’s algae, Euglena sanguinea, and/ or the genus Euglena itself, in 1830 in the cited paper, but did not diagnose the genus until 1838, according to the Euglenoid Project at Rutgers University, 2000, citing Ehrenberg 1838.
9 Contra Hort, see discussion in main text (below) and De Vaux 1978:361 fn. 5.
10 For some reason, Hort does not mention the modern calendar month she assigns to the tenth Plague, she only mentions the ancient Hebrew month named Abib or Aviv (March/April). De Vaux and LaSor, Hubbard and Bush, agree in interpreting Hort as placing the last Palgue in March or April (De Vaux 1978:361: LaSor, Hubbard and Bush 1982:140. fn. 25),
11 Hort 1957:93, Hoffmeier erroneously considers secondary elements 2, 3, and 4 (fish kill, stench, importability) as primary, that they are supposedly among Hort’s four primary Biblical conditions for identifying the Plague of Blood, and on a level comparable to the blood-red color criterion (which is actually Hort’s one and only “primary clue”) (Hoffmeier 1997:146).
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