A creole language,[1][2][3] or simply creole, is a stable natural language that develops from the simplifying and mixing of different languages at a fairly sudden point in time: often, a pidgin transitioned into a full-fledged language. While the concept is similar to that of a mixed or hybrid language, a creole is often additionally defined as being highly simplified when compared to its parent languages. However, a creole is still complex enough that it has a consistent system of grammar, possesses a large stable vocabulary, and is acquired by children as their native language, all of which distinguishes a creole language from a pidgin.
The precise number of creole languages is not known, particularly as many are poorly attested or documented. About one hundred creole languages have arisen since 1500.  These are predominantly based on European languages such as English and French[4] due to the European Age of Discovery and the Atlantic slave trade that arose at that time.[5] With the improvements in ship-building and navigation, traders had to learn to communicate with people around the world, and the quickest way to do this was to develop a pidgin, or simplified language suited to the purpose; in turn, full creole languages developed from these pidgins. In addition to creoles that have European languages as their base, there are, for example, creoles based on Arabic, Chinese, and Malay. The creole with the largest number of speakers is Haitian Creole, with almost ten million native speakers,[6] followed by Tok Pisin with about 4 million, most of whom are second-language speakers.
The lexicon (or, roughly, the base or essential vocabulary – such as "run" but not "running") of a creole language is largely supplied by the parent languages, particularly that of the most dominant group in the social context of the creole's construction. However, there are often clear phonetic and semantic shifts. On the other hand, the grammar that has evolved often has new or unique features that differ substantially from those of the parent languages.
Overview
A creole is believed to arise when a pidgin, developed by adults for use as a second language, becomes the native and primary language of their children – a process known as nativization.[7] The pidgin-creole life cycle was studied by American linguist Robert Hall in the 1960s.[8]
Some argue that creoles share more grammatical similarities with each other than with the languages from which they are phylogenetically derived.[9] However, there is no widely accepted theory that would account for those perceived similarities.[10] Moreover, no grammatical feature has been shown to be specific to creoles.[11][12][13][14][15][16]
Many of the creoles known today arose in the last 500 years, as a result of the worldwide expansion of European maritime power and trade in the Age of Discovery, which led to extensive European colonial empires. Like most non-official and minority languages, creoles have generally been regarded in popular opinion as degenerate variants or dialects of their parent languages. Because of that prejudice, many of the creoles that arose in the European colonies, having been stigmatized, have become extinct. However, political and academic changes in recent decades have improved the status of creoles, both as living languages and as object of linguistic study.[17][18] Some creoles have even been granted the status of official or semi-official languages of particular political territories.
Linguists now recognize that creole formation is a universal phenomenon, not limited to the European colonial period, and an important aspect of language evolution (see Vennemann (2003)). For example, in 1933 Sigmund Feist postulated a creole origin for the Germanic languages.[19]
Other scholars, such as Salikoko Mufwene, argue that pidgins and creoles arise independently under different circumstances, and that a pidgin need not always precede a creole nor a creole evolve from a pidgin. Pidgins, according to Mufwene, emerged in trade colonies among "users who preserved their native vernaculars for their day-to-day interactions." Creoles, meanwhile, developed in settlement colonies in which speakers of a European language, often indentured servants whose language would be far from the standard in the first place, interacted extensively with non-European slaves, absorbing certain words and features from the slaves' non-European native languages, resulting in a heavily basilectalized version of the original language. These servants and slaves would come to use the creole as an everyday vernacular, rather than merely in situations in which contact with a speaker of the superstrate was necessary.[20]
History
Origin
The English term creole comes from French créole, which is cognate with the Spanish term criollo and Portuguese crioulo, all descending from the verb criar ('to breed' or 'to raise'), all coming from Latin creare ('to produce, create').[21] The specific sense of the term was coined in the 16th and 17th century, during the great expansion in European maritime power and trade that led to the establishment of European colonies in other continents.
The terms criollo and crioulo were originally qualifiers used throughout the Spanish and Portuguese colonies to distinguish the members of an ethnic group who were born and raised locally from those who immigrated as adults. They were most commonly applied to nationals of the colonial power, e.g. to distinguish españoles criollos (people born in the colonies from Spanish ancestors) from españoles peninsulares (those born in the Iberian Peninsula, i.e. Spain). However, in Brazil the term was also used to distinguish between negros crioulos (blacks born in Brazil from African slave ancestors) and negros africanos (born in Africa). Over time, the term and its derivatives (Creole, Kréol, Kreyol, Kreyòl, Kriol, Krio, etc.) lost the generic meaning and became the proper name of many distinct ethnic groups that developed locally from immigrant communities. Originally, therefore, the term "creole language" meant the speech of any of those creole peoples.
Geographic distribution
As a consequence of colonial European trade patterns, most of the known European-based creole languages arose in coastal areas in the equatorial belt around the world, including the Americas, western Africa, Goa along the west of India, and along Southeast Asia up to Indonesia, Singapore, Macau, Hong Kong, the Philippines, Malaysia, Mauritius, Reunion, Seychelles and Oceania.[22]
Many of those creoles are now extinct, but others still survive in the Caribbean, the north and east coasts of South America (The Guyanas), western Africa, Australia (see Australian Kriol language), and in the Indian Ocean.
Atlantic Creole languages are based on European languages with elements from African and possibly Amerindian languages. Indian Ocean Creole languages are based on European languages with elements from Malagasy and possibly other Asian languages. There are, however, creoles like Nubi and Sango that are derived solely from non-European languages.
Social and political status
Because of the generally low status of the Creole peoples in the eyes of prior European colonial powers, creole languages have generally been regarded as "degenerate" languages, or at best as rudimentary "dialects" of the politically dominant parent languages. Because of this, the word "creole" was generally used by linguists in opposition to "language", rather than as a qualifier for it.[23]
Another factor that may have contributed to the relative neglect of creole languages in linguistics is that they do not fit the 19th-century neogrammarian "tree model" for the evolution of languages, and its postulated regularity of sound changes (these critics including the earliest advocates of the wave model, Johannes Schmidt and Hugo Schuchardt, the forerunners of modern sociolinguistics). This controversy of the late 19th century profoundly shaped modern approaches to the comparative method in historical linguistics and in creolistics.[17][23][24]

Because of social, political, and academic changes brought on by decolonization in the second half of the 20th century, creole languages have experienced revivals in the past few decades. They are increasingly being used in print and film, and in many cases, their community prestige has improved dramatically. In fact, some have been standardized, and are used in local schools and universities around the world.[17][18][25] At the same time, linguists have begun to come to the realization that creole languages are in no way inferior to other languages. They now use the term "creole" or "creole language" for any language suspected to have undergone creolization, terms that now imply no geographic restrictions nor ethnic prejudices.
Creolization is widely thought to be a leading influence on the evolution of African-American English (AAE).  The controversy surrounding AAVE in the American education system, as well as the past use of the word ebonics to refer to it, mirrors the historical negative connotation of the word creole.[26]
Classification
Historic classification
According to their external history, four types of creoles have been distinguished: plantation creoles, fort creoles, maroon creoles, and creolized pidgins.[27] By the very nature of a creole language, the phylogenetic classification of a particular creole usually is a matter of dispute; especially when the pidgin precursor and its parent tongues (which may have been other creoles or pidgins) have disappeared before they could be documented.
Phylogenetic classification traditionally relies on inheritance of the lexicon, especially of "core" terms, and of the grammar structure. However, in creoles, the core lexicon often has mixed origin, and the grammar is largely original. For these reasons, the issue of which language is the parent of a creole – that is, whether a language should be classified as a "Portuguese creole" or "English creole", etc. – often has no definitive answer, and can become the topic of long-lasting controversies, where social prejudices and political considerations may interfere with scientific discussion.[17][18][24]
Substrate and superstrate
The terms substrate and superstrate are often used when two languages interact. However, the meaning of these terms is reasonably well-defined only in second language acquisition or language replacement events, when the native speakers of a certain source language (the substrate) are somehow compelled to abandon it for another target language (the superstrate).[28] The outcome of such an event is that erstwhile speakers of the substrate will use some version of the superstrate, at least in more formal contexts. The substrate may survive as a second language for informal conversation. As demonstrated by the fate of many replaced European languages (such as Etruscan, Breton, and Venetian), the influence of the substrate on the official speech is often limited to pronunciation and a modest number of loanwords. The substrate might even disappear altogether without leaving any trace.[28]
However, there is dispute over the extent to which the terms "substrate" and "superstrate" are applicable to the genesis or the description of creole languages.[29] The language replacement model may not be appropriate in creole formation contexts, where the emerging language is derived from multiple languages without any one of them being imposed as a replacement for any other.[30][31] The substratum-superstratum distinction becomes awkward when multiple superstrata must be assumed (such as in Papiamentu), when the substratum cannot be identified, or when the presence or the survival of substratal evidence is inferred from mere typological analogies.[14] On the other hand, the distinction may be meaningful when the contributions of each parent language to the resulting creole can be shown to be very unequal, in a scientifically meaningful way.[32] In the literature on Atlantic Creoles, "superstrate" usually means European and "substrate" non-European or African.[33]
Decreolization
Since creole languages rarely attain official status, the speakers of a fully formed creole may eventually feel compelled to conform their speech to one of the parent languages. This decreolization process typically brings about a post-creole speech continuum characterized by large-scale variation and hypercorrection in the language.[17]
It is generally acknowledged that creoles have a simpler grammar and more internal variability than older, more established languages.[34] However, these notions are occasionally challenged.[35] (See also language complexity.)
Phylogenetic or typological comparisons of creole languages have led to divergent conclusions. Similarities are usually higher among creoles derived from related languages, such as the languages of Europe, than among broader groups that include also creoles based on non-Indo-European languages (like Nubi or Sango). French-based creoles in turn are more similar to each other (and to varieties of French) than to other European-based creoles. It was observed, in particular, that definite articles are mostly prenominal in English-based creole languages and English whereas they are generally postnominal in French creoles and in the variety of French that was exported to what is now Quebec in the 17th and 18th century.[36] Moreover, the European languages which gave rise to the creole languages of European colonies all belong to the same subgroup of Western Indo-European and have highly convergent grammars; to the point that Whorf joined them into a single Standard Average European language group.[37] French and English are particularly close, since English, through extensive borrowing, is typologically closer to French than to other Germanic languages.[38] Thus the claimed similarities between creoles may be mere consequences of similar parentage, rather than characteristic features of all creoles.
Creole genesis
There are a variety of theories on the origin of creole languages, all of which attempt to explain the similarities among them. Arends, Muysken & Smith (1995) outline a fourfold classification of explanations regarding creole genesis:
Theories focusing on European input
Theories focusing on non-European input
Gradualist and developmental hypotheses
Universalist approaches
Theories focusing on European input
Monogenetic theory of pidgins and creoles
The monogenetic theory of pidgins and creoles hypothesizes that they are all derived from a single Mediterranean Lingua Franca, via a West African Pidgin Portuguese of the 17th century, relexified in the so-called "slave factories" of Western Africa that were the source of the Atlantic slave trade. This theory was originally formulated by Hugo Schuchardt in the late 19th century and popularized in the late 1950s and early 1960s by Taylor,[39] Whinnom,[40] Thompson,[41] and Stewart.[42] However, this hypothesis is no longer actively investigated, as there are examples of creoles, such as Hezhou, which evidently have nothing to do with the Lingua Franca.
Domestic origin hypothesis
Proposed by Hancock (1985) for the origin of English-based creoles of the West Indies, the Domestic Origin Hypothesis argues that, towards the end of the 16th century, English-speaking traders began to settle in the Gambia and Sierra Leone rivers as well as in neighboring areas such as the Bullom and Sherbro coasts. These settlers intermarried with the local population leading to mixed populations, and, as a result of this intermarriage, an English pidgin was created. This pidgin was learned by slaves in slave depots, who later on took it to the West Indies and formed one component of the emerging English creoles.
European dialect origin hypothesis
The French creoles are the foremost candidates to being the outcome of "normal" linguistic change and their creoleness to be sociohistoric in nature and relative to their colonial origin.[43] Within this theoretical framework, a French creole is a language phylogenetically based on French, more specifically on a 17th-century koiné French extant in Paris, the French Atlantic harbours, and the nascent French colonies. Supporters of this hypothesis suggest that the non-Creole French dialects still spoken in many parts of the Americas share mutual descent from this single koiné. These dialects are found in Canada (mostly in Québec and in Acadian communities), Louisiana, Saint-Barthélemy and as isolates in other parts of the Americas.[44] Approaches under this hypothesis are compatible with gradualism in change and models of imperfect language transmission in koiné genesis.
Foreigner talk and baby talk
The Foreigner Talk (FT) hypothesis argues that a pidgin or creole language forms when native speakers attempt to simplify their language in order to address speakers who do not know their language at all. Because of the similarities found in this type of speech and speech directed to a small child, it is also sometimes called baby talk.[45]
Arends, Muysken & Smith (1995) suggest that four different processes are involved in creating Foreigner Talk:
Accommodation
Imitation
Telegraphic condensation
Conventions
This could explain why creole languages have much in common, while avoiding a monogenetic model. However, Hinnenkamp (1984), in analyzing German Foreigner Talk, claims that it is too inconsistent and unpredictable to provide any model for language learning.
While the simplification of input was supposed to account for creoles' simple grammar, commentators have raised a number of criticisms of this explanation:[46]
There are a great many grammatical similarities amongst pidgins and creoles despite having very different lexifier languages.
Grammatical simplification can be explained by other processes, i.e. the innate grammar of Bickerton's language bioprogram theory.
Speakers of a creole's lexifier language often fail to understand, without learning the language, the grammar of a pidgin or creole.
Pidgins are more often used amongst speakers of different substrate languages than between such speakers and those of the lexifier language.
Another problem with the FT explanation is its potential circularity. Bloomfield (1933) points out that FT is often based on the imitation of the incorrect speech of the non-natives, that is the pidgin. Therefore, one may be mistaken in assuming that the former gave rise to the latter.
Imperfect L2 learning
The imperfect L2 (second language) learning hypothesis claims that pidgins are primarily the result of the imperfect L2 learning of the dominant lexifier language by the slaves. Research on naturalistic L2 processes has revealed a number of features of "interlanguage systems" that are also seen in pidgins and creoles:
invariant verb forms derived from the infinitive or the least marked finite verb form;
loss of determiners or use as determiners of demonstrative pronouns, adjectives or adverbs;
placement of a negative particle in preverbal position;
use of adverbs to express modality;
fixed single word order with no inversion in questions;
reduced or absent nominal plural marking.
Imperfect L2 learning is compatible with other approaches, notably the European dialect origin hypothesis and the universalist models of language transmission.[47]
Theories focusing on non-European input
Theories focusing on the substrate, or non-European, languages attribute similarities amongst creoles to the similarities of African substrate languages. These features are often assumed to be transferred from the substrate language to the creole or to be preserved invariant from the substrate language in the creole through a process of relexification: the substrate language replaces the native lexical items with lexical material from the superstrate language while retaining the native grammatical categories.[48] The problem with this explanation is that the postulated substrate languages differ amongst themselves and with creoles in meaningful ways. Bickerton (1981) argues that the number and diversity of African languages and the paucity of a historical record on creole genesis makes determining lexical correspondences a matter of chance. Dillard (1970) coined the term "cafeteria principle" to refer to the practice of arbitrarily attributing features of creoles to the influence of substrate African languages or assorted substandard dialects of European languages.
For a representative debate on this issue, see the contributions to Mufwene (1993); for a more recent view, Parkvall (2000).
Because of the sociohistoric similarities amongst many (but by no means all) of the creoles, the Atlantic slave trade and the plantation system of the European colonies have been emphasized as factors by linguists such as McWhorter (1999).
Gradualist and developmental hypotheses
One class of creoles might start as pidgins, rudimentary second languages improvised for use between speakers of two or more non-intelligible native languages. Keith Whinnom (in Hymes (1971)) suggests that pidgins need three languages to form, with one (the superstrate) being clearly dominant over the others. The lexicon of a pidgin is usually small and drawn from the vocabularies of its speakers, in varying proportions. Morphological details like word inflections, which usually take years to learn, are omitted; the syntax is kept very simple, usually based on strict word order. In this initial stage, all aspects of the speech – syntax, lexicon, and pronunciation – tend to be quite variable, especially with regard to the speaker's background.
If a pidgin manages to be learned by the children of a community as a native language, it may become fixed and acquire a more complex grammar, with fixed phonology, syntax, morphology, and syntactic embedding. Pidgins can become full languages in only a single generation. "Creolization" is this second stage where the pidgin language develops into a fully developed native language. The vocabulary, too, will develop to contain more and more items according to a rationale of lexical enrichment.[49]
Universalist approaches

Universalist models stress the intervention of specific general processes during the transmission of language from generation to generation and from speaker to speaker. The process invoked varies: a general tendency towards semantic transparency, first language learning driven by universal process, or general process of discourse organization. The main universalist theory is still Bickerton's language bioprogram theory, proposed in the 1980s.[50] Bickerton claims that creoles are inventions of the children growing up on newly founded plantations. Around them, they only heard pidgins spoken, without enough structure to function as natural languages; and the children used their own innate linguistic capacities to transform the pidgin input into a full-fledged language. The alleged common features of all creoles would then be the consequence of those innate abilities being universal.
Recent studies

The last decade has seen the emergence of some new questions about the nature of creoles: in particular, the question of how complex creoles are and the question of whether creoles are indeed "exceptional" languages.
Creole prototype
Some features that distinguish creole languages from noncreoles have been proposed (by Bickerton,[51] for example).
John McWhorter[52] has proposed the following list of features to indicate a creole prototype:
a lack of inflectional morphology (other than at most two or three inflectional affixes),
a lack of tone on monosyllabic words, and
a lack of semantically opaque word formation.
McWhorter hypothesizes that these three properties exactly characterize a creole. However, the creole prototype hypothesis has been disputed:
Henri Wittmann (1999) and David Gil (2001) argue that languages such as Manding, Soninke, Magoua French and Riau Indonesian have all these three features but show none of the sociohistoric traits of creole languages.
Others (see overview in Muysken & Law (2001)) have demonstrated creoles that serve as counterexamples to McWhorter's hypothesis – the existence of inflectional morphology in Berbice Dutch Creole, for example, or tone in Papiamentu.[53]
Exceptionalism
Building up on this discussion, McWhorter proposed that "the world's simplest grammars are Creole grammars", claiming that every noncreole language's grammar is at least as complex as any creole language's grammar.[54][55] Gil has replied that Riau Indonesian has a simpler grammar than Saramaccan, the language McWhorter uses as a showcase for his theory.[13] The same objections were raised by Wittmann in his 1999 debate with McWhorter.[56]
The lack of progress made in defining creoles in terms of their morphology and syntax has led scholars such as Robert Chaudenson, Salikoko Mufwene, Michel DeGraff, and Henri Wittmann to question the value of creole as a typological class; they argue that creoles are structurally no different from any other language, and that creole is a sociohistoric concept – not a linguistic one – encompassing displaced populations and slavery.[57]
Thomason & Kaufman (1988) spell out the idea of creole exceptionalism, claiming that creole languages are an instance of nongenetic language change due to language shift with abnormal transmission. Gradualists question the abnormal transmission of languages in a creole setting and argue that the processes which created today's creole languages are no different from universal patterns of language change.
Given these objections to creole as a concept, DeGraff and others question the idea that creoles are exceptional in any meaningful way.[16][58] Additionally, Mufwene (2002) argues that some Romance languages are potential creoles but that they are not considered as such by linguists because of a historical bias against such a view.
See also
Creolistics
Dialect
Diglossia
Gradualism
Language change
Language contact
Lingua franca
List of creole languages
Macaronic language
Middle English creole hypothesis
Mixed language
Pidgin
Koine language
Nation language
Nicaraguan Sign Language
Relexification
Substratum
Creoles by parent language
Arabic-based creole languages
Assamese-based: Nagamese
Chinese-based: Tangwang, Hokaglish
Dutch-based creole languages
English-based creole languages
French-based creole languages
German-based: Unserdeutsch
Hindi-based: Andaman Creole Hindi
Japanese-based: Yilan Creole Japanese, Kanbun Kundoku[59]
Kongo-based: Kituba
Malay-based creole languages
Ngbandi-based: Sango
Portuguese-based creole languages
Spanish-based creole languages
Sinhala-based: Vedda language

Further reading

Wittmann, Henri (1999).  The Creolist Archives Papers On-line, Stockholms Universitet.
Wittmann, Henri (2001).  CreoList debate, parts I-VI, appendixes 1–9. The Linguist List, Eastern Michigan University|Wayne State University

 at Answers.com
 at the Online Dictionary of Language Terminology (ODLT)

In French

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The common cold, also known simply as a cold, is a viral infectious disease of the upper respiratory tract that primarily affects the nose.[7] The throat, sinuses, and larynx may also be affected.[5] Signs and symptoms may appear less than two days after exposure to the virus.[5] These may include coughing, sore throat, runny nose, sneezing, headache, and fever.[2][3] People usually recover in seven to ten days,[2] but some symptoms may last up to three weeks.[6] Occasionally those with other health problems may develop pneumonia.[2]

Well over 200 virus strains are implicated in causing the common cold, with rhinoviruses being the most common.[11] They spread through the air during close contact with infected people or indirectly through contact with objects in the environment, followed by transfer to the mouth or nose.[2] Risk factors include going to child care facilities, not sleeping well, and psychological stress.[5] The symptoms are mostly due to the body's immune response to the infection rather than to tissue destruction by the viruses themselves.[12] In contrast, those affected by influenza can show similar symptoms as people with a cold, but symptoms are usually more severe.[5] Additionally, influenza is less likely to result in a runny nose.[13]

There is no vaccine for the common cold.[2] The primary methods of prevention are hand washing; not touching the eyes, nose or mouth with unwashed hands; and staying away from sick people.[2] Some evidence supports the use of face masks.[14] There is also no cure, but the symptoms can be treated.[2] Zinc may reduce the duration and severity of symptoms if started shortly after the onset of symptoms.[8] Nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen may help with pain.[9] Antibiotics, however, should not be used[15] and there is no good evidence for cough medicines.[5][16]

The common cold is the most frequent infectious disease in humans.[17] The average adult gets two to three colds a year, while the average child may get six to eight.[7][10] Infections occur more commonly during the winter.[2] These infections have existed throughout human history.[18]
Signs and symptoms
The typical symptoms of a cold include a cough, a runny nose, nasal congestion and a sore throat, sometimes accompanied by muscle ache, fatigue, headache, and loss of appetite.[19] A sore throat is present in about 40% of cases and a cough in about 50%,[7] while muscle ache occurs in about half.[3] In adults, a fever is generally not present but it is common in infants and young children.[3] The cough is usually mild compared to that accompanying influenza.[3] While a cough and a fever indicate a higher likelihood of influenza in adults, a great deal of similarity exists between these two conditions.[20] A number of the viruses that cause the common cold may also result in asymptomatic infections.[21][22]
The color of the sputum or nasal secretion may vary from clear to yellow to green and does not indicate the class of agent causing the infection.[23]
Progression
A cold usually begins with fatigue, a feeling of being chilled, sneezing, and a headache, followed in a couple of days by a runny nose and cough.[19] Symptoms may begin within sixteen hours of exposure[24] and typically peak two to four days after onset.[3][25] They usually resolve in seven to ten days, but some can last for up to three weeks.[6] The average duration of cough is eighteen days[26] and in some cases people develop a post-viral cough which can linger after the infection is gone.[27] In children, the cough lasts for more than ten days in 35–40% of cases and continues for more than 25 days in 10%.[28]
Cause
Viruses

The common cold is a viral infection of the upper respiratory tract. The most commonly implicated virus is a rhinovirus (30–80%), a type of picornavirus with 99 known serotypes.[29][30] Other commonly implicated viruses include human coronavirus (≈15%),[31][32]influenza viruses (10–15%),[33] adenoviruses (5%),[33] human respiratory syncytial virus, enteroviruses other than rhinoviruses, human parainfluenza viruses, and metapneumovirus.[34] Frequently more than one virus is present.[35] In total over 200 viral types are associated with colds.[3]
Transmission
The common cold virus is typically transmitted via airborne droplets (aerosols), direct contact with infected nasal secretions, or fomites (contaminated objects).[7][36] Which of these routes is of primary importance has not been determined.[37] The viruses may survive for prolonged periods in the environment (over 18 hours for rhinoviruses) and can be picked up by people's hands and subsequently carried to their eyes or nose where infection occurs.[36] Transmission is common in daycare and at school due to the proximity of many children with little immunity and frequently poor hygiene.[38] These infections are then brought home to other members of the family.[38] There is no evidence that recirculated air during commercial flight is a method of transmission.[36] People sitting in close proximity appear to be at greater risk of infection.[37]
Rhinovirus-caused colds are most infectious during the first three days of symptoms; they are much less infectious afterwards.[39]
Weather
The traditional theory is that a cold can be "caught" by prolonged exposure to cold weather such as rain or winter conditions, which is how the disease got its name.[40] Some of the viruses that cause the common colds are seasonal, occurring more frequently during cold or wet weather.[41] The reason for the seasonality has not been conclusively determined.[42] Possible explanations may include cold temperature-induced changes in the respiratory system,[43] decreased immune response,[44] and low humidity causing an increase in viral transmission rates, perhaps due to dry air allowing small viral droplets to disperse farther and stay in the air longer.[45]
The apparent seasonality may also be due to social factors, such as people spending more time indoors, near infected people,[43] and specifically children at school.[38][42] There is some controversy over the role of low body temperature as a risk factor for the common cold; the majority of the evidence suggests that it may result in greater susceptibility to infection.[44]
Other
Herd immunity, generated from previous exposure to cold viruses, plays an important role in limiting viral spread, as seen with younger populations that have greater rates of respiratory infections.[46] Poor immune function is a risk factor for disease.[46][47] Insufficient sleep and malnutrition have been associated with a greater risk of developing infection following rhinovirus exposure; this is believed to be due to their effects on immune function.[48][49] Breast feeding decreases the risk of acute otitis media and lower respiratory tract infections among other diseases,[50] and it is recommended that breast feeding be continued when an infant has a cold.[51] In the developed world breast feeding may not be protective against the common cold in and of itself.[52]
Pathophysiology

The symptoms of the common cold are believed to be primarily related to the immune response to the virus.[12] The mechanism of this immune response is virus specific. For example, the rhinovirus is typically acquired by direct contact; it binds to human via ICAM-1 receptors and the CDHR3 receptor through unknown mechanisms to trigger the release of inflammatory mediators.[12] These inflammatory mediators then produce the symptoms.[12] It does not generally cause damage to the nasal epithelium.[3] The respiratory syncytial virus (RSV), on the other hand, is contracted by direct contact and airborne droplets. It then replicates in the nose and throat before frequently spreading to the lower respiratory tract.[53] RSV does cause epithelium damage.[53] Human parainfluenza virus typically results in inflammation of the nose, throat, and bronchi.[54] In young children when it affects the trachea it may produce the symptoms of croup due to the small size of their airways.[54]
Diagnosis
The distinction between viral upper respiratory tract infections is loosely based on the location of symptoms with the common cold affecting primarily the nose, pharyngitis (the throat), and bronchitis (the lungs).[7] There can be significant overlap and more than one area can be affected.[7] The common cold is frequently defined as nasal inflammation with varying amount of throat inflammation.[55] Self-diagnosis is frequent.[3] Isolation of the viral agent involved is rarely performed,[55] and it is generally not possible to identify the virus type through symptoms.[3]
Prevention
The only useful ways to reduce the spread of cold viruses are physical measures[14] such as hand washing and face masks; in the healthcare environment, gowns and disposable gloves are also used.[14] Isolation or quarantine is not used as the disease is so widespread and symptoms are non-specific. Vaccination has proved difficult as there are many viruses involved and they mutate rapidly.[14] Creation of a broadly effective vaccine is, thus, highly improbable.[56]
Regular hand washing appears to be effective in reducing the transmission of cold viruses, especially among children.[57] Whether the addition of antivirals or antibacterials to normal hand washing provides greater benefit is unknown.[57] Wearing face masks when around people who are infected may be beneficial; however, there is insufficient evidence for maintaining a greater social distance.[57]
It is unclear if zinc supplements affect the likelihood of contracting a cold.[58] Routine vitamin C supplements do not reduce the risk or severity of the common cold, though they may reduce its duration.[59] Gargling with water was found useful in one small trial.[60]
Management

Treatment for the common cold primarily involves medications and other therapies for symptomatic relief.[10] Getting plenty of rest, drinking fluids to maintain hydration, and gargling with warm salt water are reasonable conservative measures.[34] Much of the benefit from symptomatic treatment is, however, attributed to the placebo effect.[61] No medications or herbal remedies have been conclusively demonstrated to shorten the duration of infection.[62]
Symptomatic
Treatments that may help with symptoms include simple pain medication and medications for fevers such as ibuprofen[9] and acetaminophen (paracetamol).[63] It, however, is not clear if acetaminophen helps with symptoms.[64]  It is not known if over the counter cough medications are effective for treating an acute cough.[65] Cough medicines are not recommended for use in children due to a lack of evidence supporting effectiveness and the potential for harm.[66][67] In 2009, Canada restricted the use of over-the-counter cough and cold medication in children six years and under due to concerns regarding risks and unproven benefits.[66] The misuse of dextromethorphan (an over-the-counter cough medicine) has led to its ban in a number of countries.[68] Intranasal corticosteroids have not been found to be useful.[69]
In adults short term use of nasal decongestants may have a small benefit.[70] Antihistamines may improve symptoms in the first day or two; however, there is no longer-term benefit and they have adverse effects such as drowsiness.[71] Other decongestants such as pseudoephedrine appear effective in adults.[72][70] Ipratropium nasal spray may reduce the symptoms of a runny nose but has little effect on stuffiness.[73] The safety and effectiveness of nasal decongestant use in children is unclear.[70]
Due to lack of studies, it is not known whether increased fluid intake improves symptoms or shortens respiratory illness.[74] As of 2017 it is unclear if heated and humidified air via the RhinoTherm device was of any benefit.[75] One study has found chest vapor rub to provide some relief of nocturnal cough, congestion, and sleep difficulty.[76]
Some advise to avoid physical exercise if there are symptoms such as fever, widespread muscle aches or fatigue.[77][78] It is regarded as safe to perform moderate exercise if the symptoms are confined to the head, including runny nose, nasal congestion, sneezing, or a minor sore throat.[77][78]
Antibiotics and antivirals
Antibiotics have no effect against viral infections or against the viruses that cause the common cold.[79] Due to their side effects, antibiotics cause overall harm but are still frequently prescribed.[79][80] Some of the reasons that antibiotics are so commonly prescribed include people's expectations for them, physicians' desire to help, and the difficulty in excluding complications that may be amenable to antibiotics.[81] There are no effective antiviral drugs for the common cold even though some preliminary research has shown benefits.[10][82]
Alternative medicine
While there are many alternative treatments used for the common cold, there is insufficient scientific evidence to support the use of most.[10] As of 2018 there is insufficient evidence to recommend for or against honey.[83] As of 2015, there is tentative evidence to support nasal irrigation.[84]
Zinc supplements may shorten the duration and reduce the severity of symptoms if supplementation begins within 24hours of the onset of symptoms.[8][58][85][86] Some zinc remedies directly applied to the inside of the nose have led to the loss of the sense of smell.[87] A 2017 expert panel, however, found the evidence to be insufficient to recommend zinc's use.[16]
Vitamin C's effect on the common cold, while extensively researched, is disappointing, except in limited circumstances: specifically, individuals exercising vigorously in cold environments.[59][88] There is no firm evidence that Echinacea products provide any meaningful benefit in treating or preventing colds.[89] It is unknown if garlic is effective.[90] A single trial of vitamin D did not find benefit.[91]
Prognosis
The common cold is generally mild and self-limiting with most symptoms generally improving in a week.[7] Half of cases go away in 10days and 90% in 15days.[92] Severe complications, if they occur, are usually in the very old, the very young, or those who are immunosuppressed.[17] Secondary bacterial infections may occur resulting in sinusitis, pharyngitis, or an ear infection.[93] It is estimated that sinusitis occurs in 8% and ear infection in 30% of cases.[94]
Epidemiology
The common cold is the most common human disease[17] and affects people all over the globe.[38] Adults typically have two to three infections annually,[7] and children may have six to ten colds a year (and up to twelve colds a year for school children).[10] Rates of symptomatic infections increase in the elderly due to declining immunity.[46]
Native Americans and Inuit are more likely to be infected with colds and develop complications such as otitis media than Caucasians.[33] This may be explained by issues such as poverty and overcrowding rather than by ethnicity.[33]
History

While the cause of the common cold has only been identified since the 1950s, the disease has been with humanity throughout history.[18] Its symptoms and treatment are described in the Egyptian Ebers papyrus, the oldest existing medical text, written before the 16th century BCE.[96] The name "cold" came into use in the 16th century, due to the similarity between its symptoms and those of exposure to cold weather.[97]
In the United Kingdom, the Common Cold Unit was set up by the Medical Research Council in 1946 and it was where the rhinovirus was discovered in 1956.[98] In the 1970s, the CCU demonstrated that treatment with interferon during the incubation phase of rhinovirus infection protects somewhat against the disease,[99] but no practical treatment could be developed. The unit was closed in 1989, two years after it completed research of zinc gluconate lozenges in the prophylaxis and treatment of rhinovirus colds, the only successful treatment in the history of the unit.[100]
Society and culture
The economic impact of the common cold is not well understood in much of the world.[94] In the United States, the common cold leads to 75–100 million physician visits annually at a conservative cost estimate of $7.7 billion per year. Americans spend $2.9 billion on over-the-counter drugs and another $400 million on prescription medicines for symptom relief.[101] More than one-third of people who saw a doctor received an antibiotic prescription, which has implications for antibiotic resistance.[101] An estimated 22–189 million school days are missed annually due to a cold. As a result, parents missed 126 million workdays to stay home to care for their children. When added to the 150 million workdays missed by employees suffering from a cold, the total economic impact of cold-related work loss exceeds $20 billion per year.[34][101] This accounts for 40% of time lost from work in the United States.[102]
Research directions
Antivirals have been tested for effectiveness in the common cold; as of 2009, none had been both found effective and licensed for use.[82] There are ongoing trials of the anti-viral drug pleconaril which shows promise against picornaviruses as well as trials of BTA-798.[103] The oral form of pleconaril had  safety issues and an aerosol form is being studied.[103] DRACO, a broad-spectrum antiviral therapy, has shown preliminary effectiveness in treating rhinovirus, as well as other infectious viruses.[104]
The genomes for all known human rhinovirus strains have been sequenced.[105]

Works cited

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What is the most common form of respiratory disease in humans?


Influenza (Flu)
Types
Avian
A/H5N1 subtype
Canine
Equine
Swine
A/H1N1 subtype
Vaccines
2009 pandemic
Pandemrix
Fluzone
Influvac
Fluvax/Flucelvax/Fluad/Fluverin
Live attenuated
Optaflu
Treatment
Amantadine
Laninamivir
Oseltamivir
Peramivir
Rimantadine
Umifenovir
Vitamin D
Zanamivir
Pandemics
1918 Spanish flu
1957 Asian flu
1968–1969 Hong Kong
2009 swine
Outbreaks
1976 swine flu
2006 H5N1 India
2007 Australian equine
2007 Bernard Matthews H5N1
2008 West Bengal
2015 United States H5N2 outbreak
See also
Flu season
Influenza evolution
Influenza research
Influenza-like illness
Vaccine reformulationsvt
The 1918 influenza pandemic (January 1918– December 1920; colloquially known as Spanish flu) was an unusually deadly influenza pandemic, the first of the two pandemics involving H1N1 influenza virus.[1] It infected 500million people around the world,[2] including people on remote Pacific islands and in the Arctic, and resulted in the deaths of 50 to 100million (three to five percent of the world's population),[3] making it one of the deadliest natural disasters in human history.[4][5][6]
Infectious disease already limited life expectancy in the early 20th century. But in the first year of the pandemic, life expectancy in the United States dropped by about 12 years.[7][8][9] Most influenza outbreaks disproportionately kill juvenile, elderly, or already weakened patients but the 1918 pandemic predominantly killed previously healthy young adults.[10]
To maintain morale, wartime censors minimized early reports of illness and mortality in Germany, the United Kingdom, France, and the United States.[11][12] Papers were free to report the epidemic's effects in neutral Spain (such as the grave illness of King Alfonso XIII).[13] This created a false impression of Spain as especially hard hit,[14] thereby giving rise to the pandemic's nickname, "Spanish Flu".[15]
Scientists offer several possible explanations for the high mortality rate of the 1918 influenza pandemic. Some research suggests that the specific variant of the virus was unusually aggressive. One group of researchers recovered the virus from the bodies of frozen victims, and transfected animals with it, causing a rapidly progressive respiratory failure and death through a cytokine storm (overreaction of the body's immune system). It was postulated that the strong immune reactions of young adults ravaged the body, whereas the weaker immune systems of children and middle-aged adults resulted in fewer deaths among those groups.[16]
In 2007, analysis of medical journals from the period of the pandemic[17][18] found that the viral infection itself was not more aggressive than any previous influenza, but that the special circumstances of the epidemic (malnourishment, overcrowded medical camps and hospitals, poor hygiene) promoted bacterial superinfection that killed most of the victims, typically after a somewhat prolonged death bed.[19][20]
Historical and epidemiological data are inadequate to identify the pandemic's geographic origin.[2] It was implicated in the outbreak of encephalitis lethargica in the 1920s.[21]
History
Hypotheses about the source
The major troop staging and hospital camp in Étaples, France, was identified as being at the center of the Spanish flu by research published in 1999 by a British team, led by virologist John Oxford.[22] In late 1917, military pathologists reported the onset of a new disease with high mortality that they later recognized as the flu. The overcrowded camp and hospital— which treated thousands of victims of chemical attacks and other casualties of war— was an ideal site for the spreading of a respiratory virus; 100,000 soldiers were in transit every day. It also was home to a live piggery, and poultry were regularly brought in for food supplies from surrounding villages. Oxford and his team postulated that a significant precursor virus, harbored in birds, mutated so it could migrate to pigs that were kept near the front.[23][24] In 2018, Michael Worobey, an evolutionary biology professor at Arizona University who is examining the history of the 1918 pandemic, revealed that he obtained tissue slides created by William Rolland, a physician who reported on a respiratory illness likely to be the virus while a pathologist in the British military during World War I.[25] Rolland had authored an article in the Lancet during 1917 about a respiratory illness outbreak beginning in 1916 in Étaples, France.[26] Worobey traced recent references to that article to family members who had retained slides that Rolland had prepared during that time. Worobey is planning to extract tissue from the slides that may reveal more about the origin of the pathogen.
Nevertheless, there have been persistent claims that the epidemic originated in the United States. Historian Alfred W. Crosby claimed that the flu originated in Kansas,[27] and popular author John Barry described Haskell County, Kansas, as the point of origin.[28] It has also been claimed that, by late 1917, there had already been a first wave of the epidemic in at least 14 US military camps.[29]
Earlier hypotheses put forward varying points of origin for the epidemic. Some hypothesized that the flu originated in East Asia, a common area for transmission of disease from animals to humans because of dense living conditions.[30] Claude Hannoun, the leading expert on the 1918 flu for the Pasteur Institute, asserted the former virus was likely to have come from China, mutating in the United States near Boston and spreading to Brest, France, Europe's battlefields, Europe, and the world via Allied soldiers and sailors as the main spreaders.[31] He considered several other hypotheses of origin, such as Spain, Kansas (United States), and Brest, as being possible, but not likely.
Political scientist Andrew Price-Smith published data from the Austrian archives suggesting the influenza had earlier origins, beginning in Austria in early 1917.[32]
In 2014, historian Mark Humphries of the Memorial University of Newfoundland in St. John's stated that newly unearthed records confirmed that one of the side stories of the war, the mobilization of 96,000 Chinese laborers to work behind the British and French lines on World War I's western front, might have been the source of the pandemic. In the report, Humphries found archival evidence that a respiratory illness that struck northern China in November 1917 was identified a year later by Chinese health officials as identical to the "Spanish" flu.[33][34] A report published in 2016 in the Journal of the Chinese Medical Association found no evidence that the 1918 virus was imported to Europe via Chinese and Southeast Asian soldiers and workers. It found evidence that the virus had been circulating in the European armies for months and possibly years before the 1918 pandemic.[35]
Spread
When an infected person sneezes or coughs, more than half a million virus particles can be spread to those close by.[36] The close quarters and massive troop movements of World War I hastened the pandemic, and probably both increased transmission and augmented mutation; the war may also have increased the lethality of the virus. Some speculate the soldiers' immune systems were weakened by malnourishment, as well as the stresses of combat and chemical attacks, increasing their susceptibility.[37]
A large factor in the worldwide occurrence of this flu was increased travel. Modern transportation systems made it easier for soldiers, sailors, and civilian travelers to spread the disease.[38]
In the United States, the disease was first observed in Haskell County, Kansas, in January 1918, prompting local doctor Loring Miner to warn the U.S. Public Health Service's academic journal. On 4 March 1918, company cook Albert Gitchell reported sick at Fort Riley, an American military facility that at the time was training American troops during World War I, making him the first recorded victim of the flu.[39][40] Within days, 522 men at the camp had reported sick.[41] By 11 March 1918, the virus had reached Queens, New York.[42] Failure to take preventive measures in March/April was later criticised.[5]
In August 1918, a more virulent strain appeared simultaneously in Brest, France; in Freetown, Sierra Leone; and in the U.S. in Boston, Massachusetts. The Spanish flu also spread through Ireland, carried there by returning Irish soldiers. The Allies of World War I came to call it the Spanish flu, primarily because the pandemic received greater press attention after it moved from France to Spain in November 1918. Spain was not involved in the war and had not imposed wartime censorship.[43]
Mortality
Around the globe

The global mortality rate from the 1918/1919 pandemic is not known, but an estimated 10% to 20% of those who were infected died. With about a third of the world population infected, this case-fatality ratio means 3% to 6% of the entire global population died.[2] Influenza may have killed as many as 25million people in its first 25 weeks. Older estimates say it killed 40–50million people,[4] while current estimates say 50–100million people worldwide were killed.[46]
This pandemic has been described as "the greatest medical holocaust in history" and may have killed more people than the Black Death.[47] It is said that this flu killed more people in 24 weeks than AIDS killed in 24 years, and more in a year than the Black Death killed in a century,[16] although the Black Death killed a much higher percentage of the world's smaller population at the time.[48]
The disease killed in every area of the globe. As many as 17million people died in India, about 5% of the population.[49] The death toll in India's British-ruled districts alone was 13.88 million.[50]
In Japan, of the 23 million people who were affected, 390,000 died.[51] In the Dutch East Indies (now Indonesia), 1.5 million were assumed to have died among 30 million inhabitants.[52] In Tahiti 13% of the population died during one month. Similarly, in Samoa 22% of the population of 38,000 died within two months.[53]
In Iran, the mortality was very high: according to an estimate, between 902,400 and 2,431,000, or 8.0% to 21.7% of the total population died.[54]
In the U.S., about 28% of the population became infected, and 500,000 to 675,000 died.[55] Native American tribes were particularly hard hit. In the Four Corners area alone, 3,293 deaths were registered among Native Americans.[56] Entire Inuit and Alaskan Native village communities died in Alaska.[57] In Canada 50,000 died.[58]
In Brazil, 300,000 died, including president Rodrigues Alves.[59] In Britain, as many as 250,000 died; in France, more than 400,000.[60]
In West Africa the influenza epidemic killed at least 100,000 people in Ghana.[61] Tafari Makonnen (the future Haile Selassie, Emperor of Ethiopia) was one of the first Ethiopians who contracted influenza but survived.[62][63] Many of his subjects did not; estimates for fatalities in the capital city, Addis Ababa, range from 5,000 to 10,000, or higher.[64] In British Somaliland, one official estimated that 7% of the native population died.[65]
This huge death toll was caused by an extremely high infection rate of up to 50% and the extreme severity of the symptoms, suspected to be caused by cytokine storms.[4] Symptoms in 1918 were so unusual that initially influenza was misdiagnosed as dengue, cholera, or typhoid. One observer wrote, "One of the most striking of the complications was hemorrhage from mucous membranes, especially from the nose, stomach, and intestine. Bleeding from the ears and petechial hemorrhages in the skin also occurred".[46] The majority of deaths were from bacterial pneumonia,[66][67] a common secondary infection associated with influenza. The virus also killed people directly, by causing massive hemorrhages and edema in the lung.[67]
The unusually severe disease killed up to 20% of those infected, as opposed to the usual flu epidemic mortality rate of 0.1%.[2][46]
Patterns of fatality
The pandemic mostly killed young adults. In 1918–1919, 99% of pandemic influenza deaths in the U.S. occurred in people under 65, and nearly half in young adults 20 to 40years old. In 1920, the mortality rate among people under 65 had decreased sixfold to half the mortality rate of people over 65, but still 92% of deaths occurred in people under 65.[68] This is unusual, since influenza is normally most deadly to weak individuals, such as infants (under age two), the very old (over age 70), and the immunocompromised. In 1918, older adults may have had partial protection caused by exposure to the 1889–1890 flu pandemic, known as the Russian flu.[69]
According to historian John M. Barry, the most vulnerable of all– "those most likely, of the most likely", to die– were pregnant women. He reported that in thirteen studies of hospitalized women in the pandemic, the death rate ranged from 23% to 71%.[70]
Of the pregnant women who survived childbirth, over one-quarter (26%) lost the child.[71]
Another oddity was that the outbreak was widespread in the summer and autumn (in the Northern Hemisphere); influenza is usually worse in winter.[72]
Modern analysis has shown the virus to be particularly deadly because it triggers a cytokine storm, which ravages the stronger immune system of young adults.[28]
In fast-progressing cases, mortality was primarily from pneumonia, by virus-induced pulmonary consolidation. Slower-progressing cases featured secondary bacterial pneumonias, and there may have been neural involvement that led to mental disorders in some cases. Some deaths resulted from malnourishment.
A study– conducted by He et al.– used a mechanistic modelling approach to study the three waves of the 1918 influenza pandemic. They tried to study the factors that underlie variability in temporal patterns, and the patterns of mortality and morbidity. Their analysis suggests that temporal variations in transmission rate provide the best explanation, and the variation in transmission required to generate these three waves is within biologically plausible values.[73]
Another study by He et al. used a simple epidemic model, to incorporate three factors, including school opening and closing, temperature changes over the course of the outbreak, and human behavioral changes in response to the outbreak, to infer the cause of the three waves of the 1918 influenza pandemic. Their modelling results showed that all three factors are important but human behavioral responses showed the largest effects.[74]
Deadly second wave

The second wave of the 1918 pandemic was much deadlier than the first. The first wave had resembled typical flu epidemics; those most at risk were the sick and elderly, while younger, healthier people recovered easily. But by  August, when the second wave began in France, Sierra Leone, and the United States,[75] the virus had mutated to a much deadlier form. As the PBS American Experience: Influenza 1918 episode says, October 1918 was the deadliest month of the whole pandemic.
This increased severity has been attributed to the circumstances of the First World War.[76] In civilian life, natural selection favors a mild strain. Those who get very ill stay home, and those mildly ill continue with their lives, preferentially spreading the mild strain. In the trenches, natural selection was reversed. Soldiers with a mild strain stayed where they were, while the severely ill were sent on crowded trains to crowded field hospitals, spreading the deadlier virus. The second wave began and the flu quickly spread around the world again. Consequently, during modern pandemics, health officials pay attention when the virus reaches places with social upheaval (looking for deadlier strains of the virus).[77]
The fact that most of those who recovered from first-wave infections had become immune showed that it must have been the same strain of flu. This was most dramatically illustrated in Copenhagen, which escaped with a combined mortality rate of just 0.29% (0.02% in the first wave and 0.27% in the second wave) because of exposure to the less-lethal first wave.[78] For the rest of the population, the second wave was far more deadly; the most vulnerable people were those like the soldiers in the trenches– young previously healthy adults.[79]
Devastated communities

Even in areas where mortality was low, so many adults were incapacitated that much of everyday life was hampered. Some communities closed all stores or required customers to leave orders outside. There were reports that health-care workers could not tend the sick nor the gravediggers bury the dead because they too were ill. Mass graves were dug by steam shovel and bodies buried without coffins in many places.[80]
Several Pacific island territories were particularly hard-hit. The pandemic reached them from New Zealand, which was too slow to implement measures to prevent ships carrying the flu from leaving its ports. From New Zealand, the flu reached Tonga (killing 8% of the population), Nauru (16%) and Fiji (5%, 9,000 people).[81]
Worst affected was Western Samoa, formerly German Samoa, which had been occupied by New Zealand in 1914. 90% of the population was infected; 30% of adult men, 22% of adult women and 10% of children died. By contrast, Governor John Martin Poyer prevented the flu from reaching American Samoa by imposing a blockade.[81] The disease spread fastest through the higher social classes among the indigenous peoples, because of the custom of gathering oral tradition from chiefs on their deathbeds; many community elders were infected through this process.[82]
In New Zealand, 8,573 deaths were attributed to the 1918 pandemic influenza, resulting in a total population fatality rate of 0.74%.[83] Māori were 10 times as likely to die as pākehā (Europeans), because of their poorer and more crowded housing, and rural population.[82]
In Ireland, the Spanish Flu accounted for 10% of the total deaths in 1918.
Data analysis revealed 6,520 recorded deaths in Savannah-Chatham County, Georgia (population = 83,252) for the three-year period from January 1, 1917, to December 31, 1919. Of these deaths, influenza was specifically listed as the cause of death in 316 cases, representing 4.85 percent of all causes of death for the total time period.[84]
Less-affected areas
In Japan, 257,363 deaths were attributed to influenza by July 1919, giving an estimated 0.425% mortality rate, much lower than nearly all other Asian countries for which data are available. The Japanese government severely restricted sea travel to and from the home islands when the pandemic struck.
In the Pacific, American Samoa[85] and the French colony of New Caledonia[86] also succeeded in preventing even a single death from influenza through effective quarantines. In Australia, nearly 12,000 perished.[87]
By the end of the pandemic, the isolated island of Marajó, in Brazil's Amazon River Delta had not reported an outbreak.[88]
Saint Helena also reported no deaths.[89]
Aspirin poisoning
In a 2009 paper published in the journal Clinical Infectious Diseases, Karen Starko proposed that aspirin poisoning contributed substantially to the fatalities. She based this on the reported symptoms in those dying from the flu, as reported in the post mortem reports still available, and also the timing of the big "death spike" in October 1918. This occurred shortly after the Surgeon General of the United States Army and the Journal of the American Medical Association both recommended very large doses of 8 to 31 grams of aspirin per day as part of treatment. These levels will produce hyperventilation in 33% of patients, as well as lung edema in 3% of patients.[90] Starko also notes that many early deaths showed "wet," sometimes hemorrhagic lungs, whereas late deaths showed bacterial pneumonia. She suggests that the wave of aspirin poisonings was due to a "perfect storm" of events: Bayer's patent on aspirin expired, so many companies rushed in to make a profit and greatly increased the supply; this coincided with the Spanish flu; and the symptoms of aspirin poisoning were not known at the time.[90]
As an explanation for the universally high mortality rate, this hypothesis was questioned in a letter to the journal published in April 2010 by Andrew Noymer and Daisy Carreon of the University of California, Irvine, and Niall Johnson of the Australian Commission on Safety and Quality in Health Care. They questioned the universal applicability of the aspirin theory, given the high mortality rate in countries such as India, where there was little or no access to aspirin at the time compared to the rate where aspirin was plentiful.[91] They concluded that "the salicylate [aspirin] poisoning hypothesis [was] difficult to sustain as the primary explanation for the unusual virulence of the 1918–1919 inﬂuenza pandemic".[91] In response, Starko said there was anecdotal evidence of aspirin use in India and argued that even if aspirin over-prescription had not contributed to the high Indian mortality rate, it could still have been a factor for high rates in areas where other exacerbating factors present in India played less of a role.[92]
End of the pandemic
After the lethal second wave struck in late 1918, new cases dropped abruptly– almost to nothing after the peak in the second wave.[16] In Philadelphia, for example, 4,597 people died in the week ending 16 October, but by 11 November, influenza had almost disappeared from the city. One explanation for the rapid decline of the lethality of the disease is that doctors got better at preventing and treating the pneumonia that developed after the victims had contracted the virus; but John Barry stated in his book that researchers have found no evidence to support this.[28]
Another theory holds that the 1918 virus mutated extremely rapidly to a less lethal strain. This is a common occurrence with influenza viruses: there is a tendency for pathogenic viruses to become less lethal with time, as the hosts of more dangerous strains tend to die out[28] (see also "Deadly Second Wave", above).
Long-term effects
A 2006 study in the Journal of Political Economy found that "cohorts in utero during the pandemic displayed reduced educational attainment, increased rates of physical disability, lower income, lower socioeconomic status, and higher transfer payments compared with other birth cohorts."[93] A 2018 study found that the pandemic reduced educational attainment in populations.[94]
Legacy

Academic Andrew Price-Smith has made the argument that the virus helped tip the balance of power in the later days of the war towards the Allied cause. He provides data that the viral waves hit the Central Powers before they hit the Allied powers, and that both morbidity and mortality in Germany and Austria were considerably higher than in Britain and France.[32]
In the United States, Britain and other countries, despite the relatively high morbidity and mortality rates that resulted from the epidemic in 1918–1919, the Spanish flu began to fade from public awareness over the decades until the arrival of news about bird flu and other pandemics in the 1990s and 2000s.[95] This has led some historians to label the Spanish flu a "forgotten pandemic".[27]
Various theories of why the Spanish flu was "forgotten" include the rapid pace of the pandemic, which killed most of its victims in the United States, for example, within a period of less than nine months, resulting in limited media coverage. The general population was familiar with patterns of pandemic disease in the late 19th and early 20th centuries: typhoid, yellow fever, diphtheria, and cholera all occurred near the same time. These outbreaks probably lessened the significance of the influenza pandemic for the public.[96] In some areas, the flu was not reported on, the only mention being that of advertisements for medicines claiming to cure it.[97]
In addition, the outbreak coincided with the deaths and media focus on the First World War.[98] Another explanation involves the age group affected by the disease. The majority of fatalities, from both the war and the epidemic, were among young adults. The deaths caused by the flu may have been overlooked due to the large numbers of deaths of young men in the war or as a result of injuries. When people read the obituaries, they saw the war or postwar deaths and the deaths from the influenza side by side. Particularly in Europe, where the war's toll was extremely high, the flu may not have had a great, separate, psychological impact, or may have seemed a mere extension of the war's tragedies.[68]
The duration of the pandemic and the war could have also played a role. The disease would usually only affect a certain area for a month before leaving, while the war, which most had initially expected to end quickly, had lasted for four years by the time the pandemic struck. This left little time for the disease to have a significant impact on the economy.
Regarding global economic effects, many businesses in the entertainment and service industries suffered losses in revenue, while the health care industry reported profit gains.[99]

Historian Nancy Bristow has argued that the pandemic, when combined with the increasing number of women attending college, contributed to the success of women in the field of nursing. This was due in part to the failure of medical doctors, who were predominantly men, to contain and prevent the illness. Nursing staff, who were predominantly women, felt more inclined to celebrate the success of their patient care and less inclined to identify the spread of the disease with their own work.[100]
In Spain, sources from the period explicitly linked the Spanish flu to the cultural figure of Don Juan. The nickname for the flu, the "Naples Soldier", was adopted from Federico Romero and Guillermo Fernández Shaw's operetta, The Song of Forgetting (La canción del olvido), the protagonist of which is a stock Don Juan type. Federico Romero, one of the librettists, quipped that the play's most popular musical number, Naples Soldier, was as catchy as the flu. Davis has argued the Spanish flu–Don Juan connection served a cognitive function, allowing Spaniards to make sense of their epidemic experience by interpreting it through a familiar template, namely the Don Juan story.[101]
Spanish flu research

The origin of the Spanish flu pandemic, and the relationship between the near-simultaneous outbreaks in humans and swine, have been controversial. One hypothesis is that the virus strain originated at Fort Riley, Kansas, in viruses in poultry and swine which the fort bred for food; the soldiers were then sent from Fort Riley around the world, where they spread the disease.[102] Similarities between a reconstruction of the virus and avian viruses, combined with the human pandemic preceding the first reports of influenza in swine, led researchers to conclude the influenza virus jumped directly from birds to humans, and swine caught the disease from humans.[103][104]
Others have disagreed,[105] and more recent research has suggested the strain may have originated in a nonhuman, mammalian species.[106] An estimated date for its appearance in mammalian hosts has been put at the period 1882–1913.[107] This ancestor virus diverged about 1913–1915 into two clades (or biological groups), which gave rise to the classical swine and human H1N1 influenza lineages. The last common ancestor of human strains dates to between February 1917 and April 1918. Because pigs are more readily infected with avian influenza viruses than are humans, they were suggested as the original recipients of the virus, passing the virus to humans sometime between 1913 and 1918.
An effort to recreate the 1918 flu strain (a subtype of avian strain H1N1) was a collaboration among the Armed Forces Institute of Pathology, the USDA ARS Southeast Poultry Research Laboratory and Mount Sinai School of Medicine in New York City. The effort resulted in the announcement (on 5 October 2005) that the group had successfully determined the virus's genetic sequence, using historic tissue samples recovered by pathologist Johan Hultin from a female flu victim buried in the Alaskan permafrost and samples preserved from American soldiers.[108]
On 18 January 2007, Kobasa et al. (2007) reported that monkeys (Macaca fascicularis) infected with the recreated flu strain exhibited classic symptoms of the 1918 pandemic, and died from cytokine storms[109]—an overreaction of the immune system. This may explain why the 1918 flu had its surprising effect on younger, healthier people, as a person with a stronger immune system would potentially have a stronger overreaction.[110]
On 16 September 2008, the body of British politician and diplomat Sir Mark Sykes was exhumed to study the RNA of the flu virus in efforts to understand the genetic structure of modern H5N1 bird flu. Sykes had been buried in 1919 in a lead coffin which scientists hoped had helped preserve the virus.[111] The coffin was found to be split because of the weight of soil over it, and the cadaver was badly decomposed. Nonetheless, samples of lung and brain tissue were taken through the split, with the coffin remaining in situ in the grave during this process.[112]
In December 2008, research by Yoshihiro Kawaoka of the University of Wisconsin linked the presence of three specific genes (termed PA, PB1, and PB2) and a nucleoprotein derived from 1918 flu samples to the ability of the flu virus to invade the lungs and cause pneumonia. The combination triggered similar symptoms in animal testing.[113]
In June 2010, a team at the Mount Sinai School of Medicine reported the 2009 flu pandemic vaccine provided some cross-protection against the 1918 flu pandemic strain.[114]
One of the few things known for certain about the influenza in 1918 and for some years after was that it was, out of the laboratory, exclusively a disease of human beings.[115]
In 2013, the AIR Worldwide Research and Modeling Group "characterized the historic 1918 pandemic and estimated the effects of a similar pandemic occurring today using the AIR Pandemic Flu Model". In the model, "a modern day "Spanish flu" event would result in additional life insurance losses of between USD 15.3–27.8 billion in the United States alone", with 188,000–337,000 deaths in the United States.[116]
Gallery

Two American Red Cross nurses demonstrating treatment practices during the influenza pandemic of 1918.
Albertan farmers wearing masks to protect themselves from the flu.
Policemen wearing masks provided by the American Red Cross in Seattle, 1918
A street car conductor in Seattle in 1918 refusing to allow passengers aboard who are not wearing masks
Red Cross workers remove a flu victim in St. Louis, Missouri (1918)
Influenza ward at Walter Reed Hospital during the Spanish flu pandemic of 1918–1919
Burying flu victims, North River, Newfoundland and Labrador (1918)
1919 Tokyo, Japan
Japanese poster in 1919
Demonstration at the Red Cross Emergency Ambulance Station in Washington, D.C., during the influenza pandemic of 1918
Cavalry memorial on the hill Lueg, memory of the Bernese cavalrymen victims of the 1918 flu pandemic; Emmental, Bern, Switzerland
The Spanish flu as the Naples Soldier (Spain, 1918)
Spanish biologists and the flu microbe (Spain, 1918)

See also

Notes

Bibliography

– Open access material by the Psychiatry and Behavioral Sciences at Health Sciences Research Commons.

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Bristow, Nancy K. American Pandemic: The Lost Worlds of the 1918 Influenza Epidemic (OUP, 2012)
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 ( by Infectious Diseases Society of America and ScienceDaily, October 3, 2009)

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Further reading

Humphries, Mark Osborne. The Last Plague: Spanish Influenza and the Politics of Public Health in Canada (University of Toronto Press; 29013) examines  the public-policy impact of the 1918 epidemic, which killed 50,000 Canadians.

 on YouTube

 on stanford.edu
 US Dept. of HHS
 Largest digital collection of newspapers, archival manuscripts and interpretive essays exploring the impact of the epidemic on 50 U.S. cities (Univ. of Michigan).

 US National Archives and Records Administration– pictures and records of the time

 "American Experience" PBS.

 Annotated links to articles, books and scientific research on the 1918 influenza pandemic

 1918 newspaper account on impact of flu on Minneapolis
 University of Wisconsin– Madison, 17 January 2007

– Exposure to virus generates lifelong immune response.
– Database of influenza genomic sequences and related information.

 a comic book of the 1918 flu pandemic published by Seattle & King County Public Health
 An online exhibit from the National Museum of Health and Medicine.
 Produced by Sheffield City Council's Libraries and Archives

How many people became infected with the Spanish Flu?