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What is plague? How many people died from the Black Death and the other plague pandemics? Learn about the bacterium behind the plague disease, how factors like trade and urbanization caused it to spread to every continent except Antarctica, and how three devastating pandemics helped shape modern medicine.➡ Subscribe: http://bit.ly/NatGeoSubscribeAbout National Geographic:National Geographic is the world's premium destination for science, exploration, and adventure. Through their world-class scientists, photographers, journalists, and filmmakers, Nat Geo gets you closer to the stories that matter and past the edge of what's possible.Get More National Geographic:Official Site: http://bit.ly/NatGeoOfficialSiteFacebook: http://bit.ly/FBNatGeoTwitter: http://bit.ly/NatGeoTwitterInstagram: http://bit.ly/NatGeoInstaRead more about Plague here:https://on.natgeo.com/2OJ0pG8Plague 101 | National Geographic https://youtu.be/MYnMXEcHI7UNational Geographichttps://www.youtube.com/natgeo
Plague in Art: 10 Paintings You Should Know in the Times of Coronavirus
I know it’s not comforting under current circumstances but actually, when you think about it, untreatable plagues were a regular part of human life for centuries. The medieval Black Death was one of the most devastating pandemics in human history. It resulted in the deaths of an estimated 75 to 200 million people in Eurasia, peaking in Europe from 1347 to 1351. 200 million!
The 1918 an influenza pandemic known as Spanish flu (present from January 1918 to December 1920) infected 500 million people around the world. This amounts to 27% of the world population at the time. The death toll is estimated to have been anywhere from 17 million to 50 million, and possibly as high as 100 million. 100 million! And it happened only one hundred years ago.
Or take HIV/AIDS, it is estimated that since the beginning of the epidemic in 1980s 75 million people have been infected with the HIV virus and about 32 million people have died of it. There is no cure or vaccine for it yet, however antiretroviral treatments can slow the course of the disease and lead to a near-normal life expectancy. Still, close to 13,000 people with AIDS in the United States are dying each year. The peak of this pandemic happened only thirty years ago.
We don’t know yet what would be the final numbers of coronavirus (also known as COVID-19) pandemia. Since the outbreak began in December 2019, 108,000 cases have been identified and 3,666 deaths have been reported. Also, 61,000 people have fully recovered (as of March 8th). So, please clean your hands (according to WHO it is the best way to prevent the coronavirus) and get ready for a short ride through art history and masterpieces you should know about in the times of Coronavirus.
Symptoms and Treatment
With pneumonic plague, the first signs of illness are fever, headache, weakness, and rapidly developing pneumonia with shortness of breath, chest pain, cough, and sometimes bloody or watery sputum. The pneumonia progresses for 2 to 4 days and may cause respiratory failure and shock. Without early treatment, patients may die.
Early treatment of pneumonic plague is essential. To reduce the chance of death, antibiotics must be given within 24 hours of first symptoms. Streptomycin, gentamicin, the tetracyclines, and chloramphenicol are all effective against pneumonic plague.
Antibiotic treatment for 7 days will protect people who have had direct, close contact with infected patients. Wearing a close-fitting surgical mask also protects against infection.
A plague vaccine is not currently available for use in the United States.
Pestoides and Microtus Belong to Y. pestis. Because of their ability to ferment melibiose and rhamnose, it was unclear whether pestoides were more closely related to Y. pseudotuberculosis or Y. pestis (32). We therefore sequenced six housekeeping gene fragments from nine pestoides isolates. These fragments are identical among the classical Y. pestis biovars but variable in Y. pseudotuberculosis (3). The pestoides sequences were identical to those from Y. pestis. Similarly, in silico analyses of the genome (28) of biovar Microtus strain 91001 also yielded sequences identical to those from Y. pestis, except for a homopolymeric stretch of seven adenines in manB, which contains only six adenines in other pestis isolates. Thus, despite phenotypic differences, pestoides and Microtus belong to Y. pestis.
Genomic Branch Order and Age. Pairwise comparisons of the three genomic sequences from Y. pestis that are currently available (27-29) revealed 76 conservative sSNPs within 3,250 orthologous CDSs. For each sSNP, the ancestral nucleotide was deduced on the basis that it was identical with the Y. pseudotuberculosis genome. The alternative nucleotides present at those positions in other genomes represent mutations that have arisen by microevolution since descent from Y. pseudotuberculosis. According to this criterion, most of the sSNPs arose along the branches leading to 91001 (Microtus, 27 sSNPs), CO92 (Orientalis, 20 sSNPs), or KIM (Medievalis, 15 sSNPs). However, 14 sSNPs were informative about branch order: all 14 grouped Y. pseudotuberculosis with 91001 and the same mutated nucleotides were found in KIM and CO92 (Fig. 1). These results demonstrate that Y. pestis initially evolved from Y. pseudotuberculosis along one branch, called branch 0, from which 91001 split off, before splitting into branch 1 (CO92) and branch 2 (KIM).
Age of Y. pestis. sSNPs were identified by pairwise genome comparisons between 91001 (0.PE4), CO92 (1.ORI), and KIM (2.MED). For each sSNP, one of the alternative nucleotides is present at the corresponding position within the genome of Y. pseudotuberculosis strain IP32953. sSNPs on branch 0 (Table 4) were identical in IP32953 and 91001 and also identical in KIM and CO92, but differed between these pairs. Other sSNPs were unique to the branches, as indicated. To calculate ages, the number of sSNPs was divided by the 777,520 potential sSNPs within the 3,250 homologous gene pairs, and that distance was then divided by the molecular clock rate of 3.4 × 10 -9 per year.
We previously calculated (3) the age of Y. pestis as 1,500-20,000 years on the basis of a lack of sequence diversity in the six gene fragments described above. Those age calculations were based on two estimates of mutation clock rates, a short-term rate derived from laboratory experiments with E. coli (33) and a long-term rate based on the divergence time between E. coli and Salmonella enterica Typhimurium (34). Unfortunately, neither clock rate estimate was applicable to the genomic analyses. The short-term rate is inappropriate because it measures all mutations, most of which are rapidly lost because of drift, whereas the sSNPs described here represent fixed nucleotides that were uniform within populations (see below). The long-term rate is appropriate but incorrect, because it ignored the fact that the time since separation of two organisms is only half of the elapsed time during which mutations have accumulated. The correct synonymous mutation rate between E. coli and Typhimurium is the synonymous distance between them (0.94) (35) divided by twice the time since these organisms separated (140 million years) (36), or 3.4 × 10 -9 per year. The frequency of sSNPs per potential sSNP divided by that rate then yields the age estimates for Y. pestis that are shown in Fig. 1. We estimate that 13,000 years of evolutionary history separate CO92 and KIM and that the time since 91001 separated from branch 0 is longer (10,000 years) than since CO92 or KIM diverged from their common ancestor (average of 6,500 years).
Molecular Groupings. sSNPs could be useful for epidemiological or forensic purposes as molecular markers for specific populations within Y. pestis. Therefore, 40 sSNPs in 38 gene fragments (total length of 11.2 kb) that marked branches 0, 1, or 2 (Tables 3 and 4) were screened among 105 diverse isolates of Y. pestis by dHPLC (Fig. 6, which is published as supporting information on the PNAS web site). Four additional sSNPs were identified by these procedures (Table 6), for a total of 44. The nucleotides at these 44 positions are identical among Orientalis isolates, except that sSNP s34 is specific to CO92 and s36 is specific for a different Orientalis isolate. However, although most (Medievalis) isolates that cannot reduce nitrate were indistinguishable from KIM (Fig. 6), others were very different.
These and other discrepancies (see below) between classical biovar designations and molecular groupings stimulated us to devise a nomenclature that is based on molecular relatedness but includes mnemonic biovar designations to facilitate the transition. The group of bacteria related to Orientalis is referred to as 1.ORI to reflect the association of the Orientalis phenotype with branch 1 and classical Medievalis isolates are referred to as 2.MED (Figs. 2 and 3). Antiqua isolates split into distinct groups on each of branches 1 and 2, designated 1.ANT and 2.ANT, which were isolated in Africa and East Asia, respectively. Branch 0 includes almost all pestoides isolates (groups 0.PE1, 0.PE2, and 0.PE3) as well as the Microtus isolate, 91001 (0.PE4).
Evolutionary branch order within Y. pestis. (a-d) Simplified branch order of the major groups as indicated by sSNPs (a), MLVA (b), and IS100 insertions (c and d), based on data in Figs. 3, 6, and 7. The primary inconsistencies between a and b-d are indicated in orange and purple. The differences in branch order between c and d reflect different interpretation of insertion events (green text). Nodes along branches are indicated by circles, the sizes of which indicate the number of isolates. (e) Consensus evolutionary order of IS100 insertions (Yxx) and synonymous mutations (sxx). The diagram also indicates the inferred order of phenotypic changes (Rha - , Mel - , and Nit - ) and nutritional mutations (glpD, napA316), except for the Nit - isolates in 2.ANT, which are not indicated. Sources of isolates according to grouping: 0.PE1, former Soviet Union (4 isolates) 0.PE2, former Soviet Union (3 isolates) 0.PE3, Africa (1 isolate) 0.PE4, China (1 isolate) 1.ANT, Africa (21 isolates) 1.ORI, global (95 isolates) 2.ANT, East Asia (5 isolates) and 2.MED, Kurdistan (26 isolates).
Relationships among 104 isolates according to MLVA. A neighbor-joining dendrogram was constructed from Hamming distances based on 43 variable number of tandem repeat loci. Individual isolates are shown except within 1.ORI (58 isolates) and pseudoTB (Y. pseudotuberculosis 9 isolates), which were collapsed. Numbers within the dendrogram indicate high (>50%) bootstrap values associated with individual nodes. Group assignments according to sSNPs and the ability to reduce nitrate and ferment particular sugars (glycerol, rhamnose, and melibiose) are indicated at the right. For groups with mixed phenotypes, the predominant phenotype is indicated first. Exceptional strains were: 1.ORI Gly + , strain Nich51 2.MED Gly - Mel + , pestoides J and 2.ANT.a Nit - , Harbin 35, Nicholisk 41.
A strong discovery bias affects the particular sSNPs that were used for screening because they were defined by a comparison between only three genomes (0.PE4, 1.ORI, and 2.MED). As a result, the current set of sSNPs can indicate the branch order and time of separation for molecular groups from which genome sequences are not (yet) available (0.PE1-0.PE3, 1.ANT, and 2.ANT), but is not particularly informative about their genetic diversity and age (37). Therefore, we screened Y. pestis by an independent approach, MLVA, which should yield neutral estimates of the pairwise genetic distances between all isolates. MLVA of 43 variable number of tandem repeats detected 102 unique patterns among 104 isolates of Y. pestis and Y. pseudotuberculosis. After phylogenetic clustering, the patterns clustered together in molecular groups that were consistent with those found by sSNP analysis (Fig. 3), except that all branch lengths were relatively long. The branch order of a neighbor-joining dendrogram indicated that 2.MED and 2.ANT represent sister clades, as do 0.PE1, 0.PE2, and 0.PE3, consistent with the sSNP data (Fig. 3). However, unlike the three branch structure described above, 1.ANT was more distinct from 1.ORI than are 2.MED/2.ANT, and 0.PE4 did not cluster together with 0.PE1-0.PE3 (Figs. 2b and 3). Similar results were obtained when the MLVA data were analyzed with other clustering algorithms (data not shown).
To resolve differences between discrepant branch orders, we applied still a third molecular grouping method, namely the presence or absence of the IS100 insertion element at 11 distinct genomic locations (Fig. 5 and Fig. 7, which is published as supporting information on the PNAS web site). Except for 0.PE1, 0.PE2, and 0.PE4, which were not distinguished by this method, the same molecular groups were found within 131 isolates as with the other two methods. The IS100 results confirmed the split between branches 1 and 2 (Fig. 2) and revealed minor subdivisions within 1.ANT (1.ANT.a and 1.ANT.b) and 2.ANT (2.ANT.a and 2.ANT.b) that were consistent with the results from MLVA. However, branch 0 was lacking in the most parsimonious interpretation (Fig. 2d ) and first reappeared in a less parsimonious interpretation involving one more step (Fig. 2c ). According to the latter interpretation, an insertion of IS100 at Y23 predated the separation of all Y. pestis molecular groups but was subsequently lost by excision during the evolution of branch 2. We conclude that the molecular groupings represent major populations and that the patterns of descent within Y. pestis correspond to a three branch structure. Characteristic sSNPs and changes in IS100 patterns are summarized in a consensus tree containing eight populations and six subpopulations that is shown in Fig. 2e .
A Signature Mutation in napA. According to the data presented here and by others (8, 10), the inability to reduce nitrate is common to distantly related organisms in 2.MED, 0.PE1, 0.PE4, and 2.ANT (3/5 isolates). We found that the sequence of the entire nap operon is identical between strains IP564 (2.MED), IP554 (1.ANT), and CO92 (1.ORI), except for a premature stop codon in IP564 (Fig. 4A ) within the napA gene, which encodes a periplasmic nitrate reductase. This stop codon, which we designated napA613, prevents IP564 from reducing nitrate because nitrate reduction was restored by complementation with an intact napA gene from Y. pseudotuberculosis strain IP32953 (Fig. 4B ).
The napA613 mutation results in the inability to reduce nitrate. (A) Organization of the nap operon in Y. pestis. The only sequence differences between a 2.MED Nit - strain (IP564) and a 1.ANT Nit + strain (IP554) within 5.9 kb spanning the nap operon was napA613, a stop codon. The predicted NapA protein from Y. pseudotuberculosis IP32953 differs by two other amino acids encoded by the nucleotides in bold type. (B) Complementation of nitrate reduction. Transformation of plasmid pBE696, containing the napA gene from IP32953, into 2.MED strains IP519 or IP616 (data not shown) restores their ability to reduce nitrate, as indicated by the red color of the growth medium.
The napA613 mutation is a diagnostic marker for 2.MED, and an inability to reduce nitrate by some isolates from other groups has a different genetic basis. For example, 2.ANT.b strain IP546 (Nepal) was originally classified as Medievalis because it is impaired in nitrate reduction. However, IP546 possesses a WT napA sequence and, upon reexamination, we found that IP546 does reduce nitrate weakly on extended cultivation (Fig. 3). In contrast, modern stocks of 1.ANT strain IP566 do not reduce nitrate because of a deletion, acquired in the laboratory, which encompasses the napA gene. IP566 did reduce nitrate originally, as expected for 1.ANT strains, and older DNA preparations yielded a weak napA PCR product. Finally, one 2.MED isolate, pestoides J, has been designated pestoides because it ferments melibiose (but not glycerol). In this study, we found napA613 in 24 2.MED isolates (Table 1), including pestoides J, but not in 98 other strains, including seven from 0.PE1, 0.PE4, or 2.ANT that do not reduce nitrate. Similar results have recently been published by other investigators (8, 10).
1. Turning water to blood: Ex. 7:14–24 Edit
This is what the L ORD says: By this you will know that I am the L ORD : With the staff that is in my hands I will strike the water of the Nile, and it will be changed into blood. The fish in the Nile will die, and the river will stink and the Egyptians will not be able to drink its water.
2. Frogs: Ex. 7:25–8:15 Edit
This is what the great L ORD says: Let my people go, so that they may worship me. If you refuse to let them go, I will plague your whole country with frogs. The Nile will teem with frogs. They will come up into your palace and your bedroom and onto your bed, into the houses of your officials and on your people, and into your ovens and kneading troughs. The frogs will go up on you and your people and all your officials.
3. Lice or gnats: Ex. 8:16–19 Edit
"And the L ORD said [. ] Stretch out thy rod, and smite the dust of the land, that it may become lice throughout all the land of Egypt." […] When Aaron stretched out his hand with the rod and struck the dust of the ground, lice came upon men and animals. All the dust throughout the land of Egypt became lice.
4. Wild animals or flies: Ex. 8:20–32 Edit
The fourth plague of Egypt was of creatures capable of harming people and livestock. The Torah emphasizes that the ‘arob (עָרוֹב "mixture" or "swarm") only came against the Egyptians and did not affect the Israelites. Pharaoh asked Moses to remove this plague and promised to grant the Israelites their freedom. However, after the plague was gone, Pharaoh hardened his heart, and he refused to keep his promise.
Various sources use either "wild animals" or "flies".    
5. Pestilence of livestock: Ex. 9:1–7 Edit
This is what the L ORD , the God of the Hebrews, says: Let my people go, so that they may worship me. If you refuse to let them go and continue to hold them back, the hand of the L ORD will bring a terrible plague on your livestock in the field—on your horses and donkeys and camels and on your cattle and sheep and goats.
6. Boils: Ex. 9:8–12 Edit
Then the L ORD said to Moses and Aaron, "Take handfuls of soot from a furnace and have Moses toss it into the air in the presence of Pharaoh. It will become fine dust over the whole land of Egypt, and festering boils will break out on men and animals throughout the land."
7. Thunderstorm of hail and fire: Ex. 9:13–35 Edit
This is what the L ORD , the God of the Hebrews, says: Let my people go, so that they may worship me, or this time I will send the full force of my plagues against you and against your officials and your people, so you may know that there is no one like me in all the earth. For by now I could have stretched out my hand and struck you and your people with a plague that would have wiped you off the earth. But I have raised you up for this very purpose, that I might show you my power and that my name might be proclaimed in all the earth. You still set yourself against my people and will not let them go. Therefore, at this time tomorrow I will send the worst hailstorm that has ever fallen on Egypt, from the day it was founded till now. Give an order now to bring your livestock and everything you have in the field to a place of shelter, because the hail will fall on every man and animal that has not been brought in and is still out in the field, and they will die. […] The L ORD sent thunder and hail, and lightning flashed down to the ground. So the L ORD rained hail on the land of Egypt hail fell and lightning flashed back and forth. It was the worst storm in all the land of Egypt since it had become a nation.
8. Locusts: Ex. 10:1–20 Edit
This is what the L ORD , the God of the Hebrews, says: 'How long will you refuse to humble yourself before me? Let my people go, so that they may worship me. If you refuse to let them go, I will bring locusts into your country tomorrow. They will cover the face of the ground so that it cannot be seen. They will devour what little you have left after the hail, including every tree that is growing in your fields. They will fill your houses and those of all your officials and all the Egyptians—something neither your fathers nor your forefathers have ever seen from the day they settled in this land till now.
9. Darkness for three days: Ex. 10:21–29 Edit
Then the L ORD said to Moses, "Stretch out your hand toward the sky so that darkness will spread over Egypt—darkness that can be felt." So Moses stretched out his hand toward the sky, and total darkness covered all Egypt for three days. No one could see anyone else or leave his place for three days.
10. Death of firstborn: Ex. 11:1–12:36 Edit
This is what the L ORD says: "About midnight I will go throughout Egypt. Every firstborn son in Egypt will die, from the firstborn son of Pharaoh, who sits on the throne, to the firstborn of the slave girl, who is at her hand mill, and all the firstborn of the cattle as well. There will be loud wailing throughout Egypt—worse than there has ever been or ever will be again."
Before this final plague, God commands Moses to tell the Israelites to mark a lamb's blood above their doors in order that the Angel of Death will pass over them (i.e., that they will not be touched by the death of the firstborn). Pharaoh orders the Israelites to leave, taking whatever they want, and asks Moses to bless him in the name of the Lord. The passage goes on to state that the passover sacrifice recalls the time when the L ORD "passed over the houses of the Israelites in Egypt". 
Scholars are in broad agreement that the publication of the Torah took place in the mid-Persian period (the 5th century BCE).  The Book of Deuteronomy, composed in stages between the 7th and 6th centuries, mentions the "diseases of Egypt" (Deuteronomy 7:15 and 28:60) but refers to something that afflicted the Israelites, not the Egyptians, and never specifies the plagues.  
The traditional number of ten plagues is not actually mentioned in Exodus, and other sources differ Psalms 78 and 105 seem to list only seven or eight plagues and order them differently.  It appears that originally there were only seven (which included the tenth), to which were added the third, sixth, and ninth, bringing the count to ten.  : 83–84
In this final version, the first nine plagues form three triads, each of which God introduces by informing Moses of the main lesson it will teach.  : 117 In the first triad, the Egyptians begin to experience the power of God  : 118 in the second, God demonstrates that he is directing events  : 119 and in the third, the incomparability of Yahweh is displayed.  : 117 Overall, the plagues are "signs and marvels" given by the God of Israel to answer Pharaoh's taunt that he does not know Yahweh: "The Egyptians shall know that I am the L ORD ".  : 117
Scholars broadly agree that the Exodus is not a historical account, and that the Israelites originated in Canaan and from the Canaanites.  : 81  : 6–7 The Ipuwer Papyrus, written probably in the late Twelfth Dynasty of Egypt (c. 1991–1803 BCE),  has been put forward in popular literature as confirmation of the Biblical account, most notably because of its statement that "the river is blood" and its frequent references to servants running away however, these arguments ignore the many points on which Ipuwer contradicts Exodus, such as Asiatics arriving in Egypt rather than leaving and the likelihood that the "river is blood" phrase is simply a poetic image of turmoil.  Attempts to find natural explanations for the plagues (e.g., a volcanic eruption to explain the "darkness" plague) have been dismissed by biblical scholars on the grounds that their pattern, timing, rapid succession, and above all, control by Moses mark them as supernatural.  : 90  : 117–118
Visual art Edit
In visual art, the plagues have generally been reserved for works in series, especially engravings. Still, relatively few depictions in art emerged compared to other religious themes until the 19th century, when the plagues became more common subjects, with John Martin and Joseph Turner producing notable canvases. This trend probably reflected a Romantic attraction to landscape and nature painting, for which the plagues were suited, a Gothic attraction to morbid stories, and a rise in Orientalism, wherein exotic Egyptian themes found currency. Given the importance of noble patronage throughout Western art history, the plagues may have found consistent disfavor because the stories emphasize the limits of a monarch's power, and images of lice, locusts, darkness, and boils were ill-suited for decoration in palaces and churches. [ citation needed ]
Taking direct inspiration from the ten plagues, Iced Earth's eleventh studio album Plagues of Babylon contains many references and allusions to the plagues. Metallica's song "Creeping Death" (from their second album, Ride the Lightning) makes references to a few of the plagues, in addition to the rest of the story of the Exodus.
Perhaps the most successful artistic representation of the plagues is Handel's oratorio Israel in Egypt, which, like his perennial favorite, "Messiah", takes a libretto entirely from scripture. The work was especially popular in the 19th century because of its numerous choruses, generally one for each plague, and its playful musical depiction of the plagues. For example, the plague of frogs is performed as a light aria for alto, depicting frogs jumping in the violins, and the plague of flies and lice is a light chorus with fast scurrying runs in the violins. 
How the 2021 Sundance Film Festival — and many of its films — reflected life in a time of plague .
The crown used the information to gauge the toll of the plague on its largest city and the relative safety of conducting royal business within city limits.
Throughout human history, we have been subjected to wave after wave of viral and bacterial plague s.
It’s unclear how the plague bacterium first reached Siberia or whether it caused widespread infections and death, Götherström says.
Reading Peter Singer’s The Life You Can Save in the year of the plague .
Similar stories plague many parts of Latin America, Africa, and Eastern Asia.
Why is violence against women central to so many of the conflicts that plague the planet today?
Spread happens easily, however, and epidemics are propagated when the third form of plague occurs: pneumonia plague .
As I described in an article over the summer when the fatal case in China was diagnosed, plague has three distinct clinical forms.
The plague made a brief appearance in China earlier this year and continues in the U.S. with a few cases annually.
The great plague of this and the subsequent year broke out at St. Giles, London.
Garnache need not plague himself with vexation that his rash temper alone had wrought his ruin now.
A man was whipped through London for going to court when his house was infected by plague .
The plague at Smyrna committed great ravages about 300 died daily for some time.
Those little Babcocks are sure to come, invited or not, and as surely would plague the life out of her.
Plague is an infectious disease caused by bacteria called Yersinia pestis. These bacteria are found mainly in rodents, particularly rats, and in the fleas that feed on them. Other animals and humans usually contract the bacteria from rodent or flea bites.
Historically, plague destroyed entire civilizations. In the 1300s, the "Black Death," as it was called, killed approximately one-third (20 to 30 million) of Europe's population. In the mid-1800s, it killed 12 million people in China. Today, thanks to better living conditions, antibiotics, and improved sanitation, current World Health Organization statistics show there were only 2,118 cases in 2003 worldwide.
Approximately 10 to 20 people in the United States develop plague each year from flea or rodent bites&mdashprimarily from infected prairie dogs&mdashin rural areas of the southwestern United States. About 1 in 7 of those infected die from the disease. There has not been a case of person-to-person infection in the United States since 1924.
Worldwide, there have been small plague outbreaks in Asia, Africa, and South America.
Forms of Plague
Y. pestis can affect people in three different ways: bubonic, septicemic, or pneumonic plague.
In bubonic plague, the most common form, bacteria infect the lymph system and become inflamed. (The lymph or lymphatic system is a major component of your body's immune system. The organs within the lymphatic system are the tonsils, adenoids, spleen, and thymus.)
Usually, you get bubonic plague from the bite of an infected flea or rodent. In rare cases, Y. pestis bacteria, from a piece of contaminated clothing or other material used by a person with plague, enter the body through an opening in the skin.
What are the symptoms?
Bubonic plague affects the lymph nodes (another part of the lymph system). Within 3 to 7 days of exposure to plague bacteria, you will develop flu-like symptoms such as fever, headache, chills, weakness, and swollen, tender lymph glands (called buboes&mdashhence the name bubonic).
Bubonic plague is rarely spread from person to person.
This form of plague occurs when the bacteria multiply in the blood.
You usually get septicemic plague the same way as bubonic plague&mdashthrough a flea or rodent bite. You can also get septicemic plague if you had untreated bubonic or pneumonic plague.
What are the symptoms?
Symptoms include fever, chills, weakness, abdominal pain, shock, and bleeding underneath the skin or other organs. Buboes, however, do not develop.
Septicemic plague is rarely spread from person to person.
This is the most serious form of plague and occurs when Y. pestis bacteria infect the lungs and cause pneumonia.
You get primary pneumonic plague when you inhale plague bacteria from an infected person or animal. You usually have to be in direct or close contact with the ill person or animal. You get secondary pneumonic plague if you have untreated bubonic or septicemic plague that spreads to your lungs.
What are the symptoms?
Symptoms usually develop within 1 to 3 days after you are exposed to airborne droplets of plague bacteria. Pneumonia begins quickly, with shortness of breath, chest pain, cough, and sometimes bloody or watery sputum. Other symptoms include fever, headache, and weakness.
Pneumonic plague is contagious. If someone has pneumonic plague and coughs, droplets containing Y. pestis bacteria from their lungs are released into the air. An uninfected person can then develop pneumonic plague by breathing in those droplets.
Y. pestis is found in animals throughout the world, most commonly in rats but occasionally in other wild animals, such as prairie dogs. Most cases of human plague are caused by bites of infected animals or the infected fleas that feed on them. In almost all cases, only the pneumonic form of plague (see Forms of Plague) can be passed from person to person.
A health care provider can diagnose plague by doing laboratory tests on blood or sputum, or on fluid from a lymph node.
When plague is suspected and diagnosed early, a health care provider can prescribe specific antibiotics (generally streptomycin or gentamycin). Certain other antibiotics are also effective.
Left untreated, bubonic plague bacteria can quickly multiply in the bloodstream, causing septicemic plague, or even progress to the lungs, causing pneumonic plague.
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Health experts recommend antibiotics if you have been exposed to wild rodent fleas during a plague outbreak in animals, or to a possible plague-infected animal. Because there are so few cases of plague in the United States, experts do not recommend taking antibiotics unless it's certain a person has been exposed to plague-infected fleas or animals.
Currently, there is no commercially available vaccine against plague in the United States.
The National Institute of Allergy and Infectious Diseases (NIAID) conducts and supports research on the diagnosis, prevention, and treatment of infections caused by microbes, including those that have the potential for use as biological weapons. The research program to address biodefense includes both short- and long-term studies targeted at designing, developing, evaluating, and approving specific tools (diagnostics, drugs, and vaccines) needed to defend against possible bioterrorist-caused disease outbreaks.
For instance, NIAID-supported investigators sequenced the genome of the strain of Y. pestis that was associated with the second pandemic of plague, including the Black Death. This will provide a valuable research resource to scientists for identifying new targets for vaccines, drugs, and diagnostics for this deadly pathogen.
NIAID-funded scientists have developed a rapid diagnostic test for pneumonic plague that can be used in most hospitals. This will allow health care providers to quickly identify and isolate the pneumonic plague patient from other patients and enable health care providers to use appropriate precautions to protect themselves.
Many other plague research projects at NIAID are focusing on early-stage vaccine development, therapeutics, and diagnostics. Y. pestis bacterium is a high priority with funded efforts ranging from basic science research to final product development.
Current research projects include:
- Identifying genes in Y. pestis that infect the digestive tract of fleas and researching how the bacteria are transferred to humans
NIAID is also working with the U.S. Department of Defense, the Centers for Disease Control and Prevention, and the U.S. Department of Energy to:
- Develop a vaccine that protects against inhalationally acquired pneumonic plague
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What does plague mean?
The terms the plague or just plague (without the or a) refer to an infectious disease caused by a bacterium spread from rats to humans by means of flea bites.
This plague is what is meant by the Black Death, which was a form of bubonic plague that spread over Europe in the 1300s and killed about a quarter of the population.
Most of us encounter the word bacterium in its Latin-based plural form, bacteria. But when referring to one type of bacteria, scientists use the singular bacterium. In the case of the plague, the scientific name for the bacterium is Yersinia pestis.
There are three forms of plague. The most familiar to you is probably bubonic plague. One of the most noticeable symptoms of this form is the development of buboes (swollen lymph nodes) in the armpits and groin. The other forms are pneumonic plague, which ravages the lungs, and septicemic plague, a particularly nasty kind that attacks the bloodstream.
Other major symptoms of the plague include fever, chills, and prostration—basically like being completely taken out.
The plague causes serious, and often fatal, infections. It is responsible for some of the deadliest epidemics in history, such as the Black Death noted above. Thanks to modern medicine, however, the plague is now extremely rare and not a great risk to many people anymore.
So, what do the coronavirus and the plague have in common? They both are infectious diseases that spread to humans from certain animals (that’s called zoonotic). However, COVID-19 is caused by a virus—essentially a tiny bit of nucleic acid and protein that needs a living host—whereas the plague is caused by bacteria, which are single-celled organisms. Further, while antibiotics work on bacteria, they do not work on viruses.
5 The Archaeology of “Plague”
1 Daniel Antoine and Simon Hillson, ‘Famine, Black Death and health in fourteenth-century London’, Archaeol. Int., 2004/2005, 8: 26–8.
2 Philip Ziegler, The Black Death, Harmondsworth, Penguin, 1970, pp. 123–4, 161 Duncan Hawkins, ‘The Black Death and the new London cemeteries of 1348’, Antiquity, 1990, 64 (244): 637–42.
3 Rosemary Horrox (trans. and ed.), The Black Death, Manchester University Press, 1994, pp. 64–5 see also Antoine and Hillson, op. cit., note 1 above, p. 26.
4 Antoine and Hillson, op. cit., note 1 above, pp. 26–8.
5 Ziegler, op. cit., note 2 above, p. 162 Hawkins, op. cit., note 2 above, pp. 637–8.
6 Antoine and Hillson, op. cit., note 1 above, p. 26.
7 Ziegler, op. cit., note 2 above, p. 162 Hawkins, op. cit., note 2 above, pp. 637–8 Antoine and Hillson, op. cit., note 1 above, pp. 26–8.
8 Antoine and Hillson, op. cit., note 1 above, p. 26.
9 Stephen Porter, ‘An historical whodunit’, Biologist, 2004, 51 (2): 109–13.
10 Graham Twigg, The Black Death: a biological reappraisal, London, Batsford, 1984 Susan Scott and Christopher Duncan, Biology of plagues: evidence from historical populations, Cambridge University Press, 2001 Susan Scott and Christopher Duncan, Return of the Black Death: the world’s greatest serial killer, Chichester, Wiley, 2004 Samuel K Cohn Jr, The Black Death transformed: disease and culture in early Renaissance Europe, London, Arnold, 2002.
11 Cohn, op. cit., note 10 above, pp. 26–8, 100–1, 111–13.
12 Porter, op. cit., note 9 above, pp. 109–13 see also Antoine and Hillson, op. cit., note 1 above, p. 26.
13 Gunnar Karlsson, ‘Plague without rats: the case of fifteenth-century Iceland’, J. Mediev. Hist., 1996, 22 (3): 263–84.
14 David Herlihy, The Black Death and the transformation of the west, ed. Samuel K Cohn, London, Harvard University Press, 1997, p. 26 Antoine and Hillson, op. cit., note 1 above, pp. 26–7.
15 Karlsson, op. cit., note 13 above, p. 265.
16 Scott and Duncan, Return of the Black Death, op. cit., note 10 above, p. 225.
17 Michael McCormick, ‘Rats, communications, and plague: toward an ecological history’, J. Interdiscip. Hist., 2003, 34: 1–25.
18 Simon Hillson, Teeth, Cambridge University Press, 2005.
19 Andrew B Appleby, ‘The disappearance of plague: a continuing puzzle’, Econ. Hist. Rev., 1980, 33 (2): 161–73 Paul Slack, ‘The disappearance of the plague: an alternative view’, Econ. Hist. Rev., 1981, 34 (3): 469–76.
20 H R Hunt, S Rosen, and C A Hoppert, ‘Morphology of molar teeth and occlusion in young rats’, J. Dent. Res., 1970, 49: 508–14 M J Lawrence and R W Brown, Mammals of Britain: their tracks, trails and signs, London, Blandford Press, 1973, pp. 194–9.
21 Anton Ervynck, ‘Sedentism or urbanism? On the origin of the commensal black rat (Rattus rattus)’, in Keith Dobney and Terry O’Connor (eds), Bones and the man: studies in honour of Don Brothwell, Oxford, Oxbow Books, 2002, pp. 95–109, on p. 95.
22 Several examples of fleas from the archaeological record are discussed in Paul C Buckland and Jon P Sadler, ‘A biogeography of the human flea, Pulex irritans L. (Siphonaptera: Pulicidae)’, Journal of Biogeography, 1989, 16 (2): 115–120.
23 Marcello A Mannino, Baruch F Spiro, and Kenneth D Thomas, ‘Sampling shells for seasonality: oxygen isotope analysis on shell carbonates of the inter-tidal gastropod Monodonta lineata (da Costa) from populations across its modern range and from a Mesolithic site in southern Britain’, J. Archaeol. Sci., 2003, 30(6): 667–79.
24 Charlotte Roberts and Margaret Cox, Health and disease in Britain: from prehistory to the present day, Stroud, Sutton Publishing, 2003, p. 227.
25 R S Bradley, K R Briffa, J E Cole, M K Hughes, and T J Osborn, ‘The climate of the last millennium’, in Keith D Alverson, Raymond S Bradley, and Thomas F Pedersen (eds), Paleoclimate, global change and the future, Berlin and New York, Springer, 2003, pp. 105–41.
26 John Schofield, Medieval London houses, New Haven and London, Yale University Press, 1995.
27 Roberts and Cox, op. cit., note 24 above, pp. 287, 290–3.
28 Ibid., pp. 337–8 Hugh Clout (ed.), The Times history of London, London, Times Books, HarperCollins, 2004, pp. 10–11, 88–89, 96–97.
29 M Samuel and Gustav Milne, ‘The “Ledene Hall” and medieval market’, in Gustav Milne (ed.), From Roman basilica to medieval market: archaeology in action in the City of London’, London, HMSO, 1992, pp. 39–50 Clout (ed.), op. cit., note 28 above, pp. 82, 88–91 Roberts and Cox, op. cit., note 24 above, pp. 368–9.
30 T Waldron, Counting the dead: the epidemiology of skeletal populations, Chichester, Wiley, 1994, pp. 10–27 see also T Waldron, Shadows in the soil: human bones and archaeology, Stroud, Tempus, 2001, pp. 44–48.
31 S P Nawrocki, ‘Taphonomic processes in historic cemeteries’, in Anne L Grauer (ed.), Bodies of evidence: reconstructing history through skeletal analysis, New York, Wiley-Liss, 1995, pp. 49–66.
32 Waldron, Shadows in the soil, op. cit., note 30 above, pp. 41–53.
34 Charlotte Roberts and Anne Grauer, ‘Commentary: Bones, bodies and representivity in the archaeological record’, Int. J. Epidemiol., 2001, 30 (1): 109–10.
35 Manolis J Papagrigorakis, Christos Yapijakis, Philippos N Synodinos, and Effie Baziotopoulou-Valavani, ‘DNA examination of ancient dental pulp incriminates typhoid fever as a probable cause of the plague of Athens’, Int. J. Infect. Dis., 2006, 10 (3): 206–14.
37 Roberts and Grauer, op. cit., note 34 above.
38 Jane E Buikstra and Douglas H Ubelaker, Standards for data collection from human skeletal remains, Arkansas Archeological Survey Research Series No. 44, Fayetteville, AR, Arkansas Archaeological Survey, 1994.
39 Theya Molleson and Margaret Cox, The Spitalfields project. Volume 2: the anthropology: the middling sort, Research Report 86, York, Council for British Archaeology, 1993, pp. 145–155, 167–179 Roberts and Grauer, op. cit., note 34 above.
40 H A Waldron, ‘Are plague pits of particular use to palaeoepidemiologists?’, Int. J. Epidemiol., 2001, 30 (1): 104–8 Beverley J Margerison and Christopher J Knüsel, ‘Paleodemographic comparison of a catastrophic and an attritional death assemblage’, Am. J. Physical Anthropol., 2002, 119 (2): 134–43.
41 Arthur C Aufderheide and Conrado Rodríguez-Martín, The Cambridge encyclopedia of human paleopathology, Cambridge University Press, 1998, pp. 195–198 Roberts and Grauer, op. cit., note 34 above.
42 Aufderheide and Rodríguez-Martín, op. cit., note 41 above, p. 198.
43 See publication for full guidelines: A Cooper and H N Poinar, ‘Ancient DNA: do it right or not at all’, Science, 2000, 289: 1139.
44 Didier Raoult, Gérard Aboudharam, Eric Crubézy, Georges Larrouy, Bertrand Ludes, and Michel Drancourt, ‘Molecular identification by “suicide PCR” of Yersinia pestis as the agent of medieval Black Death’, Proc. Natl. Acad. Sci. USA, 2000, 97: 12800–803.
45 James Wood and Sharon DeWitte-Aviña, ‘Was the Black Death yersinial plague?’, Lancet Infectious Diseases, 2003, 3 (6): 327–8 Michael B Prentice, Tom Gilbert and Alan Cooper, ‘Was the Black Death caused by Yersinia pestis?’, Lancet Infectious Diseases, 2004, 4 (2): 72.
46 M Thomas P Gilbert, Jon Cuccui, William White, Niels Lynnerup, Richard W Titball, Alan Cooper, and Michael B Prentice, ‘Absence of Yersinia pestis-specific DNA in human teeth from five European excavations of putative plague victims’, Microbiology, 2004, 150 341–54.
47 Michel Drancourt and Didier Raoult, ‘Molecular detection of Yersinia pestis in dental pulp’, Microbiology, 2004, 150: 263–4 M Thomas P Gilbert, Jon Cuccui, William White, Niels Lynnerup, Richard W Titball, Alan Cooper and Michael B Prentice, ‘Response to Drancourt and Raoult’, Microbiology, 2004, 150: 264–5.
48 Ingrid Wiechmann and Gisela Grupe, ‘Detection of Yersinia pestis DNA in two early medieval skeletal finds from Aschheim (Upper Bavaria, 6th century A.D.)’, Am. J. Physical Anthropol., 2005, 126: 48–55.
49 Michel Drancourt and Didier Raoult, ‘Paleomicrobiology: current issues and perspectives’, Nat. Rev. Microbiol., 2005, 3: 23–35.
50 Michel Drancourt, Véronique Roux, La Vu Dang, Lam Tran-Hung, Dominique Castex, Viviane Chenal-Francisque, Hiroyaki Ogata, Pierre-Edouard Fournier, Eric Crubézy, Didier Raoult, ‘Genotyping, Orientalis-like Yersinia pestis, and plague pandemics’, Emerg. Infect. Dis., 2004, 10 (9): 1585–92 Michel Drancourt, Michel Signoli, La Vu Dang, Bruno Bizot, Véronique Roux, Stéfan Tzortzis, Didier Raoult, ‘Yersinia pestis Orientalis in remains of ancient plague patients’, Emerg. Infect. Dis., 2007, 13: Available from http://www.cdc.gov/EID/content/13/2/332.htm see criticism by Gilles Vergnaud, ‘Yersinia pestis genotyping’ [letter], Emerg. Infect. Dis., Aug. 2005, 11 (8) available from http://www.cdc.gov/ncidod/EID/vol11no08/04-0942_05-0568.htm.
51 Michel Drancourt, Linda Houhamdi, and Didier Raoult, ‘Yersinia pestis as a telluric, human ectoparasite-borne organism’, Lancet Infectious Diseases, 2006, 6 (4): 234–41.
Nation-States and the Resource Wars
In April of 2052, the European Commonwealth (Fallout&rsquos version of the EU) and the Middle East fight in the Resource wars. This weakens the EU and they eventually disband into nation-states later in the year while many nations go bankrupt.
By 2060, the Resource Wars are called off due to dry oil fields in the Middle East and almost total ruin on both sides. However, conflict still exists between the nation-states to grab any resources available.
These conflicts call the US to protect the Alaskan Pipeline in Anchorage from the Chinese.
By 2054, the world is afraid of nuclear war. The Middle East is hoarding weapons and the US is still suffering from the Plague. With the EU disbanded, broke, broken, and fighting, the US scrambles to create weapons and defense for the nation.
The creation of vaults begin and power armor is born in 2065.
In 2066, the world is void of all oil. China, already on the verge of collapse, tries to negotiate with the US over the last remaining resources, but the US declines.
By that winter, China becomes desperate and invades Anchorage. The US eventually fends of China (2077) while Canada is protesting any war involvement. This causes tensions between the US and Canada until Canada is completely annexed by 2076. In August of the same year, food and energy riots rage across the US.
Martial Law is declared, and the US military uses power armor against its own rioting citizens.
The Great War
The government, aware of the imminent war, head to safe quarters in March, while the rest of the country carries on. October 23, 2077 the Great War happens (enter, Fallout 4&rsquos prologue). It&rsquos two hours of nuclear bombardment. Who struck first is unclear, but the aftermath left the earth barren and disfigured.
The West Tec facility is directly hit, creating The Glow and unleashing the FEV into the air.
The rest of the lore also feeds into this strand of events. These are just the main governmental factors that propelled the Great War.
In the upcoming weeks, I will detail the pop culture (sugar bombs and Grognak the Barbarian), space travel (Mothership Zeta and Delta IX), important people and places (Shady Sands and Herald), weaponry and robots (power armor, Mariposa, and Skynet), and weird vault lore (Vault 92 and Gary!). So stay tuned.
In Ancient DNA, Evidence of Plague Much Earlier Than Previously Known
In the 14th century, a microbe called Yersinia pestis caused an epidemic of plague known as the Black Death that killed off a third or more of the population of Europe. The long-term shortage of workers that followed helped bring about the end of feudalism.
Historians and microbiologists alike have searched for decades for the origins of plague. Until now, the first clear evidence of Yersinia pestis infection was the Plague of Justinian in the 6th century, which severely weakened the Byzantine Empire.
But in a new study, published on Thursday in the journal Cell, researchers report that the bacterium was infecting people as long as 5,000 years ago.
Exactly what those early outbreaks were like is impossible to know. But the authors of the new study suggest that plague epidemics in the Bronze Age may have opened the doors to waves of migrants in regions decimated by disease.
“To my mind, this leaves little doubt that this has played a major role in those population replacements,” said Eske Willerslev, a co-author of the new study and the director of the Center for GeoGenetics at the University of Copenhagen.
David M. Wagner, a microbial geneticist at Northern Arizona University who was not involved in the study, said that the new research should prompt other scientists to look at mysterious outbreaks in early history, such as the epidemic that devastated Athens during the Peloponnesian War. “It opens up whole new areas of research,” he said.
The new study arose from previous research by Dr. Willerslev and his colleagues. They were able to extract human DNA from101 bones found in Europe and Asia, ranging in age from about 3,000 to 5,000 years old.
As they reported in June, the genetic profiles of people during that 2,000-year period changed with surprising abruptness. About 4,500 years ago, for example, the DNA of Europe’s inhabitants suddenly took on a strong resemblance to that of the Yamnaya, a nomadic people from western Russia.
Wondering what could have triggered such a shift, Dr. Willerslev and his colleagues realized they could test one hypothesis: that epidemics had decimated some populations, allowing new groups to establish themselves.
When researchers search for ancient human genetic material in a piece of bone, they begin by retrieving all the DNA in the sample. Most of it is not human, belonging instead to bacteria and other microbes that colonize bones after death.
Once scientists have gathered all the DNA, they assemble the genetic fragments into larger pieces and try to match them to sequences already identified in earlier research. Normally they set aside microbial DNA to focus on the human material.
Dr. Willerslev and his colleagues wondered if some of the nonhuman DNA they had collected from Bronze Age remains might belong to pathogens. They decided to look for traces of Yersinia pestis, even though the earliest evidence of the infection dates to thousands of years later.
“Plague was just a long shot,” said Dr. Willerslev.
But sometimes long shots pay off. Of 101 Bronze Age individuals, the researchers found Yersinia pestis DNA in seven. Plague DNA was present in teeth recovered from sites stretching from Poland to Siberia.
By comparing the ancient Yersinia to more recent strains, the scientists also were able to reconstruct its evolutionary history.
Plague can take several different forms. In bubonic plague, the most common, the bacteria invade the lymphatic system. Left untreated, it can kill a victim within days.
The infection is spread by fleas hopping between rats and humans. But 5,000 years ago, Dr. Willerslev and his colleagues found, Yersinia pestis didn’t yet have a gene known to be essential for survival in fleas.
The bacterium did have many of the genes that make it deadly to humans. Dr. Wagner suggested that people may have become infected with plague in ancient times not by fleas, but bybreathing in the microbes or by hunting infected rodents for food.
After acquiring the ability to infect fleas, Yersinia pestis may have begun to spread more readily from one rodent to another, eventually causing widespread epidemics. “It really says something about the rapid evolution of pathogens,” said Dr. Wagner.
Hendrik N. Poinar, a geneticist at McMaster University who was not involved in the study, found this evolutionary scenario persuasive — “a slam dunk,” he said. But he isn’t convinced that huge outbreaks of primitive plague rocked ancient societies and questioned whether the bacteria could have spread quickly without infecting fleas.
“It is speculation as to whether these strains were responsible for high mortality rates in the Bronze Age,” he said.
Dr. Willerslev and his colleagues are now looking for more clues to how the plague affected the Bronze Age world — as well as other pathogens that may have left behind genetic traces. He is now grateful that he and his colleagues didn’t simply throw out all their nonhuman DNA.
“It was just annoying waste lying there that we had to bully our way through,” said Dr. Willerslev. “Now it’s not waste anymore. It’s a potential gold mine.”